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1.
Belmont, Judson.
Technologies for Phosphoproteomic Interrogation of T Cell
Signaling.
Degree: Department of Molecular Biology, Cell Biology and
Biochemistry, 2017, Brown University
URL: https://repository.library.brown.edu/studio/item/bdr:792636/
► The ability to detect and adapt to changing conditions and circumstances is a requirement of life at both the organismal and cellular levels. Inside the…
(more)
▼ The ability to detect and adapt to changing conditions
and circumstances is a requirement of life at both the organismal
and cellular levels. Inside the cell, rapid and fine-tuned
responses to environmental cues can be achieved through dynamic
post-translational modifications (PTMs) of proteins. Significant
insights into the activity and dependencies of signaling pathways
can therefore be gleaned from global surveys of PTM events, and in
particular protein phosphorylation, as it is absolutely essential
in the signaling cascades mediating the downstream functions of
receptor tyrosine kinase systems. In
T cells, coordinated
phosphorylation of tyrosine residues is critical for transmission
of signals from the activated
T cell receptor. Investigations into
the dynamic phosphoproteome of
T cells have been greatly assisted
by advances in mass spectrometry, which allows for the
identification and quantitation of thousands of PTMs simultaneously
without a requirement for site-specific antibodies. However,
despite the increasing resolution and decreasing cost of mass
spectrometry assays, the complex network of phosphorylation events
governing
T cell activation has been only incompletely
characterized. In particular, while it is now appreciated that
numerous feedback pathways within the
T cell phosphoproteome work
together to regulate the initiation of immune responses, when and
where feedback loops occur in the pathway is poorly understood. To
better understand the role that critical
T cell signaling
components play in feedback regulation of the
T cell receptor
pathway, we conducted a phosphoproteomic study into the role of
Phospholipase C-γ1 in mediating the activation state of the
receptor-proximal signaling machinery. Additionally, we
investigated the application of optimized chromatography
configurations to
T cell phosphoproteomics, and demonstrated the
immense potential to achieve greater qualitative and quantitative
insights into the
T cell signaling machinery. Finally, to support
the visualization, management, annotation, and analysis of this
proteomic data, we designed and implemented new tools to expedite
discoveries from large LC-MS datasets. The
subject of this work is
therefore the insights we have gained into the mechanisms governing
T cell activation and regulation as well as the technical and
technological innovations that made those insights
possible.
Advisors/Committee Members: Salomon, Art (Advisor), Gruppuso, Philip (Reader), de Graffenreid, Christopher (Reader), Neretti, Nicola (Reader), Gerber, Scott (Reader).
Subjects/Keywords: T cells
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Chicago ·
MLA ·
Vancouver ·
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APA (6th Edition):
Belmont, J. (2017). Technologies for Phosphoproteomic Interrogation of T Cell
Signaling. (Thesis). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:792636/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Belmont, Judson. “Technologies for Phosphoproteomic Interrogation of T Cell
Signaling.” 2017. Thesis, Brown University. Accessed March 04, 2021.
https://repository.library.brown.edu/studio/item/bdr:792636/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Belmont, Judson. “Technologies for Phosphoproteomic Interrogation of T Cell
Signaling.” 2017. Web. 04 Mar 2021.
Vancouver:
Belmont J. Technologies for Phosphoproteomic Interrogation of T Cell
Signaling. [Internet] [Thesis]. Brown University; 2017. [cited 2021 Mar 04].
Available from: https://repository.library.brown.edu/studio/item/bdr:792636/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Belmont J. Technologies for Phosphoproteomic Interrogation of T Cell
Signaling. [Thesis]. Brown University; 2017. Available from: https://repository.library.brown.edu/studio/item/bdr:792636/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Oxford
2.
Nguyen, John.
Quantitative modelling of T cell activation and co-stimulation.
Degree: PhD, 2020, University of Oxford
URL: http://ora.ox.ac.uk/objects/uuid:2b713d2d-171c-4575-874c-6ad253a74484
;
https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.808385
► Precisely regulated activity of T cells is crucial to effectively control pathogens while limiting immunopathology to a minimum. Even though T cell activation is predominantly…
(more)
▼ Precisely regulated activity of T cells is crucial to effectively control pathogens while limiting immunopathology to a minimum. Even though T cell activation is predominantly governed by antigen recognition through the T cell receptor (TCR), the activity of an array of various accessory receptors can markedly alter this decision-making process, with the potential to serve as attractive therapeutic intervention points. Therefore, many of these co-stimulatory and co-inhibitory receptors and their molecular signalling pathways have been characterised. However, how exactly these receptors integrate with TCR signalling to affect the T cell response quantitatively remains poorly understood. Here, we used in vitro expanded primary human T cells in a minimal stimulation platform to study co-stimulation through receptors of the TNF receptor superfamily (TNFRSF) in isolation. This allowed us to precisely define the ligand doses and stimulation times in order to capture the quantitative effects of TNFRSF signalling on the T cell cytokine response, with a particular focus on two representative TNFRSF members, 4-1BB and CD27. We found that 4-1BB costimulation was able to prolong the cytokine response, while engagement of CD27 increased the amount of cytokine produced without affecting the duration of the response and the T cells still became unresponsive after 8 hours. However, in combination with computational modelling, detailed analysis of our results showed that the distinct phenotypes of these receptors were mainly caused by their differential expression pattern in time, while the TNFRSF members share a common co-stimulatory mechanism, which we summarised in a minimal mathematical model. Simulations of the model predicted that co-stimulation through either of 4-1BB and CD27 could rescue TCR-dependent cytokine production in T cells which had become unresponsive through previous stimulation, and that CD27 could increase the potency of 4-1BB by enhancing its expression. We were then able to validate the model by confirming the both the rescue of the response and the synergy between TNFRSF members experimentally.
Subjects/Keywords: immunology; T cells
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Nguyen, J. (2020). Quantitative modelling of T cell activation and co-stimulation. (Doctoral Dissertation). University of Oxford. Retrieved from http://ora.ox.ac.uk/objects/uuid:2b713d2d-171c-4575-874c-6ad253a74484 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.808385
Chicago Manual of Style (16th Edition):
Nguyen, John. “Quantitative modelling of T cell activation and co-stimulation.” 2020. Doctoral Dissertation, University of Oxford. Accessed March 04, 2021.
http://ora.ox.ac.uk/objects/uuid:2b713d2d-171c-4575-874c-6ad253a74484 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.808385.
MLA Handbook (7th Edition):
Nguyen, John. “Quantitative modelling of T cell activation and co-stimulation.” 2020. Web. 04 Mar 2021.
Vancouver:
Nguyen J. Quantitative modelling of T cell activation and co-stimulation. [Internet] [Doctoral dissertation]. University of Oxford; 2020. [cited 2021 Mar 04].
Available from: http://ora.ox.ac.uk/objects/uuid:2b713d2d-171c-4575-874c-6ad253a74484 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.808385.
Council of Science Editors:
Nguyen J. Quantitative modelling of T cell activation and co-stimulation. [Doctoral Dissertation]. University of Oxford; 2020. Available from: http://ora.ox.ac.uk/objects/uuid:2b713d2d-171c-4575-874c-6ad253a74484 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.808385
3.
Nevers, Tania A.
Inflammatory and dysfunctional regulatory T cells in adverse
pregnancy outcomes.
Degree: PhD, Pathobiology, 2012, Brown University
URL: https://repository.library.brown.edu/studio/item/bdr:297562/
► The etiologies for adverse pregnancy outcomes such as recurrent spontaneous abortion, preeclampsia, preterm birth and gestational diabetes mellitus (GDM) are multi-factorial and remain poorly understood.…
(more)
▼ The etiologies for adverse pregnancy outcomes such as
recurrent spontaneous abortion, preeclampsia, preterm birth and
gestational diabetes mellitus (GDM) are multi-factorial and remain
poorly understood. The main reasons for enigmatic state of adverse
pregnancy outcomes can be assigned to lack of well defined animal
models in response to inflammatory triggers and early pregnancy
predictive assays and biomarkers. However, these pregnancy
complications have a common contributor in inflammation at the
maternal-fetal interface. In normal pregnancy, a state of immune
tolerance is choreographed involving pro- and anti-inflammatory
signals. Regulatory
T cells (Tregs) have acquired a premier role in
regulating immune tolerance systemically and at the maternal-fetal
interface. Here we focus on Tregs for their phenotypic and
functional dysregulation in mouse and human models of pregnancy
complications. Importantly, we invoke the role of IL-10, a
signature cytokine of Tregs, and human chorionic gonadotropin (hCG)
in maintaining normal pregnancy. Our overarching hypothesis is that
uterine regulatory
T cells are dysfunctional in adverse pregnancies
associated with infection and /or inflammation and may be
normalized by IL-10 and hCG.
This work explores dysregulation of uterine Tregs by
utilizing mouse models of adverse pregnancies, human peripheral
blood Tregs and sera from normal pregnancy, preeclampsia and
gestational diabetes. In Chapter 2, we show that uterine regulatory
T cells amplify and acquire an inflammatory phenotype in response
to the TLR-3 agonist and cause pregnancy demise in IL-10-/- and
wild-type (WT) mice. In Chapter 3, we present for the first time
that peripheral blood Tregs from GDM patients present an
“exhausted” phenotype and express the programmed death receptor
(PD-1). Tregs from GDM lose CD25 and Foxp3 expression upon
overnight culturing which can be partially rescued by TGF-β, IL-2,
or PD-1 blockade. This phenotype was not observed in Tregs from
normal pregnancy. In Chapter 4, we describe that hCG produced in
preeclampsia is inactive and does not support angiogenesis and
recruitment of Tregs to the uterus in the “humanized” mouse model
of preeclampsia. Collectively, the results presented in this thesis
provide novel pathways by which regulatory
T cells can present
themselves as foes of normal pregnancy.
Advisors/Committee Members: Sharma, Surendra (Director), Ayala, alfred (Reader), Fast, Loren (Reader), Reichner, Jonathan (Reader), Golos, Thaddeus (Reader).
Subjects/Keywords: Regulatory T cells
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Nevers, T. A. (2012). Inflammatory and dysfunctional regulatory T cells in adverse
pregnancy outcomes. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:297562/
Chicago Manual of Style (16th Edition):
Nevers, Tania A. “Inflammatory and dysfunctional regulatory T cells in adverse
pregnancy outcomes.” 2012. Doctoral Dissertation, Brown University. Accessed March 04, 2021.
https://repository.library.brown.edu/studio/item/bdr:297562/.
MLA Handbook (7th Edition):
Nevers, Tania A. “Inflammatory and dysfunctional regulatory T cells in adverse
pregnancy outcomes.” 2012. Web. 04 Mar 2021.
Vancouver:
Nevers TA. Inflammatory and dysfunctional regulatory T cells in adverse
pregnancy outcomes. [Internet] [Doctoral dissertation]. Brown University; 2012. [cited 2021 Mar 04].
Available from: https://repository.library.brown.edu/studio/item/bdr:297562/.
Council of Science Editors:
Nevers TA. Inflammatory and dysfunctional regulatory T cells in adverse
pregnancy outcomes. [Doctoral Dissertation]. Brown University; 2012. Available from: https://repository.library.brown.edu/studio/item/bdr:297562/
4.
Ruiz, Victoria E.
Immune response to Helicobacter pylori infection in the
gastric cancer prone p27-deficient mouse model.
Degree: PhD, Pathobiology, 2012, Brown University
URL: https://repository.library.brown.edu/studio/item/bdr:297572/
► Helicobacter pylori infection is associated with severe chronic inflammation, however the host immune response is unable to clear the bacterium. Thymus derived lymphocyte populations such…
(more)
▼ Helicobacter pylori infection is associated with
severe chronic inflammation, however the host immune response is
unable to clear the bacterium. Thymus derived lymphocyte
populations such as
T-helper 1,
T-helper 17, and
T-regulatory
lymphocytes are known to promote chronicity of infection as well as
increased gastric pathology. It is yet to be established how these
immune
cells interact in the gastric environment during H. pylori
infection and how changes in the gastric
T- lymphocyte cell
repertoire may lead gastric cancer associated pathology.
To first characterize gastric
T-lymphocyte populations, a
gastric lymphocyte isolation technique was developed. H. pylori
infected murine gastric tissue was digested with EDTA/DTT and
collagenase IV. To enrich for gastric lymphocyte populations, a
lympholyte M gradient was used. This protocol successfully isolated
1x 106 viable lymphocytes from the gastric compartment to be used
for ex vivo experiments and subsequent immunophenotyping using flow
cytometric analysis. Using this procedure a 2-fold increase of CD8+
IFNg-expressing lymphocytes was observed in the gastric compartment
during H. pylori infection.
Implementing the established gastric lymphocyte isolation
technique, gastric
T-helper and
T-regulatory lymphocyte populations
were evaluated in p27-deficient mice. These mice develop gastric
cancer a year after H. pylori infection, mimicking the human
clinical course of disease. Thus providing a suitable model to
study H. pylori induced immunopathogenesis. This work demonstrated
that H. pylori infected p27-deficient mice displayed an increased
frequency of CD4+ IFNγ+
T helper populations in the stomach, spleen
and mesenteric lymph nodes. Additionally, infected p27-deficient
mice exhibited elevated protein and transcript levels of
pro-inflammatory cytokines IFNγ, TNFα, ΙL-12p40 and chemokine,
RANTES. Along with a significant Th-1 skewed response,
p27-deficient mice exhibited decreased H. pylori colonization and
increased gastric pathology compared to its wild-type counterparts.
This data demonstrates that in p27-deficient mice, H. pylori
induces a pro-inflammatory environment by recruiting Th1
cells to
the gastric mucosa and other lymphoid compartments. Data suggest
that this recruitment, likely mediated by RANTES, may contribute to
subsequent gastric pathogenesis and eventual bacterial clearance.
Advisors/Committee Members: Moss, Steven (Director), Ayala, Alfred (Reader), Fast, Loren (Reader), Salazar-Mather, Thais (Reader), Perez-Perez, Guillermo (Reader).
Subjects/Keywords: T-helper cells
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Ruiz, V. E. (2012). Immune response to Helicobacter pylori infection in the
gastric cancer prone p27-deficient mouse model. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:297572/
Chicago Manual of Style (16th Edition):
Ruiz, Victoria E. “Immune response to Helicobacter pylori infection in the
gastric cancer prone p27-deficient mouse model.” 2012. Doctoral Dissertation, Brown University. Accessed March 04, 2021.
https://repository.library.brown.edu/studio/item/bdr:297572/.
MLA Handbook (7th Edition):
Ruiz, Victoria E. “Immune response to Helicobacter pylori infection in the
gastric cancer prone p27-deficient mouse model.” 2012. Web. 04 Mar 2021.
Vancouver:
Ruiz VE. Immune response to Helicobacter pylori infection in the
gastric cancer prone p27-deficient mouse model. [Internet] [Doctoral dissertation]. Brown University; 2012. [cited 2021 Mar 04].
Available from: https://repository.library.brown.edu/studio/item/bdr:297572/.
Council of Science Editors:
Ruiz VE. Immune response to Helicobacter pylori infection in the
gastric cancer prone p27-deficient mouse model. [Doctoral Dissertation]. Brown University; 2012. Available from: https://repository.library.brown.edu/studio/item/bdr:297572/

University of Oxford
5.
Kurioka, Ayako.
Mucosal associated invariant T cells and CD161 expressing natural killer cells.
Degree: PhD, 2015, University of Oxford
URL: https://ora.ox.ac.uk/objects/uuid:f994e661-d241-4a1c-ac56-b6bea73346ac
;
https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.730591
► Mucosal-associated invariant T (MAIT) cells are a population of innate-like lymphocytes within the gut, liver and blood, expressing a semi-invariant T cell receptor (TCR) and…
(more)
▼ Mucosal-associated invariant T (MAIT) cells are a population of innate-like lymphocytes within the gut, liver and blood, expressing a semi-invariant T cell receptor (TCR) and high levels of the C-type lectin-like receptor, CD161. These cells recognise a metabolite of the microbial riboflavin synthesis pathway, presented by the highly conserved Major Histocompatibility Complex (MHC) class I-related protein, MR1, and are critical for the control of bacterial infections. The factors regulating the broad effector functions of MAIT cells have not been fully investigated. Utilising a novel flow cytometric killing assay, MAIT cells were shown here to require the induction of a cytotoxic phenotype through bacterial stimulation to efficiently kill target cells. Further in depth phenotypic analysis highlighted a distinct non-cytotoxic subset of CD4+ MAIT cells, with an altered cytokine-producing capacity, enriched within lymphoid tissues. Investigation into the potential role of these cells in psoriatic diseases revealed that MAIT cells within the synovial fluid of psoriatic arthritis patients are potently activated with increased IL-17 production, their frequency correlating with measures of clinical activity. MAIT cells also have an innate-like responsiveness to cytokines, a feature originally attributed to Natural Killer (NK) cells. Microarray analysis and mass cytometry experiments demonstrated that CD161 marks immature NK cells that have retained this ability to respond to innate cytokines during their differentiation, and is lost upon cytomegalovirus (CMV)-induced maturation in both healthy and human immunodeficiency virus (HIV)-infected patients. Thus, CD161 marks cells with innate-effector functions both in T cells and NK cells.
Subjects/Keywords: 616.07; T cells
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Kurioka, A. (2015). Mucosal associated invariant T cells and CD161 expressing natural killer cells. (Doctoral Dissertation). University of Oxford. Retrieved from https://ora.ox.ac.uk/objects/uuid:f994e661-d241-4a1c-ac56-b6bea73346ac ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.730591
Chicago Manual of Style (16th Edition):
Kurioka, Ayako. “Mucosal associated invariant T cells and CD161 expressing natural killer cells.” 2015. Doctoral Dissertation, University of Oxford. Accessed March 04, 2021.
https://ora.ox.ac.uk/objects/uuid:f994e661-d241-4a1c-ac56-b6bea73346ac ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.730591.
MLA Handbook (7th Edition):
Kurioka, Ayako. “Mucosal associated invariant T cells and CD161 expressing natural killer cells.” 2015. Web. 04 Mar 2021.
Vancouver:
Kurioka A. Mucosal associated invariant T cells and CD161 expressing natural killer cells. [Internet] [Doctoral dissertation]. University of Oxford; 2015. [cited 2021 Mar 04].
Available from: https://ora.ox.ac.uk/objects/uuid:f994e661-d241-4a1c-ac56-b6bea73346ac ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.730591.
Council of Science Editors:
Kurioka A. Mucosal associated invariant T cells and CD161 expressing natural killer cells. [Doctoral Dissertation]. University of Oxford; 2015. Available from: https://ora.ox.ac.uk/objects/uuid:f994e661-d241-4a1c-ac56-b6bea73346ac ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.730591

University of Gothenburg / Göteborgs Universitet
6.
Alsén, Samuel.
Dendritic cells and B cells in effector T cells decisions - promotion of antibody induction in lymphoid tissues or gut homing.
Degree: 2018, University of Gothenburg / Göteborgs Universitet
URL: http://hdl.handle.net/2077/55393
► Abstract CD4+ T cells are principal cells of the adaptive immune system, equipped with the ability to boost innate immune cells and aid B cells…
(more)
▼ Abstract
CD4+ T cells are principal cells of the adaptive immune system, equipped with the ability to boost innate immune cells and aid B cells in the germinal centers. Every T cell clone carries a variable and unique T cell receptor that recognizes a protein-derived peptide presented on MHC molecules by antigen presenting cells (APC) in secondary lymphoid organs. Dendritic cells (DC) are the most prominent APC due to their unmatched ability to internalize foreign protein antigens, degrade them into peptides, load peptides onto MHC molecules and migrate to lymph nodes and present the antigen to T cells. Recognition of its cognate antigen leads to activation and proliferation of T cells while additional co-stimulatory signals dictate the differentiation and fate of T cells. Although T effector cell differentiation can be induced during the first encounter with an APC, the differentiation of B cell supporting T follicular helper (Tfh) cells require continuous antigen presentation by B cells. These two differentiation pathways of T cells occur in parallel and are guided by reciprocal antagonistic transcription factors. Herein, we have studied how APCs, with a focus on DCs and B cells, influence T cell differentiation.
By adoptively transferring CD4+ T cells with a known antigen specificity into recipient transgenic mice in which DCs can be depleted we show Tfh differentiation in the absence of DCs as long as a sufficient amount of antigen is administered together with the adjuvant. However, depletion of DCs lead to a loss of Th1 effector T cells that had downstream consequences on B cells by preventing class-switching into the Th1-associated antibody isotype. Excluding the altered class-switch, germinal center B cells showed normal affinity maturation and memory formation. This shows that Tfh cells generated in the absence of DCs are fully functional and that DCs therefore do not provide unique accessory signals required for Tfh differentiation.
T cells that differentiate to develop into Tfh cells become programmed to do so already during the primary encounter with an APC. To fulfill the Tfh differentiation program pre-Tfh cells must then interact with antigen presenting B cells to fully adopt Tfh functionality. This step-wise process has been extensively studied but it still remains unclear precisely how B cells enforce the Tfh program. In the second and third study, we exploited mixed bone marrow chimeras to generate mice in which B cells cannot present antigens to T cell thus terminating the Tfh program at the stage of T-B interactions.
In these studies, we reveal a role of B cells in regulating T cell expression of IL-4, its receptor IL4R and a H2-Q2, a gene previously not described in T cell biology. We also show that B cells affect the output of T effector cells from the lymph node. In lymph, we identify T cells that exhibit phenotypic characteristics of Tfh cells, show a history of IL-4 secretion and are dependent on cognate B cell interactions. Some of these migratory ex-Tfh cells show gut tropism and can be…
Subjects/Keywords: Immunology; T cells; T follicular helper cells; dendritic cells
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Alsén, S. (2018). Dendritic cells and B cells in effector T cells decisions - promotion of antibody induction in lymphoid tissues or gut homing. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/55393
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Alsén, Samuel. “Dendritic cells and B cells in effector T cells decisions - promotion of antibody induction in lymphoid tissues or gut homing.” 2018. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed March 04, 2021.
http://hdl.handle.net/2077/55393.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Alsén, Samuel. “Dendritic cells and B cells in effector T cells decisions - promotion of antibody induction in lymphoid tissues or gut homing.” 2018. Web. 04 Mar 2021.
Vancouver:
Alsén S. Dendritic cells and B cells in effector T cells decisions - promotion of antibody induction in lymphoid tissues or gut homing. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2018. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/2077/55393.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Alsén S. Dendritic cells and B cells in effector T cells decisions - promotion of antibody induction in lymphoid tissues or gut homing. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2018. Available from: http://hdl.handle.net/2077/55393
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Queen Mary, University of London
7.
Kishore, Madhav.
The role of co-stimulatory receptors in the regulation of regulatory T cell migration.
Degree: PhD, 2016, Queen Mary, University of London
URL: http://qmro.qmul.ac.uk/xmlui/handle/123456789/12869
;
https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.775244
► Once an immune response is initiated, a combination of several mechanisms coordinates and directs the homing of T cells to their target tissue. Co-stimulatory receptors…
(more)
▼ Once an immune response is initiated, a combination of several mechanisms coordinates and directs the homing of T cells to their target tissue. Co-stimulatory receptors expressed on the surface of T lymphocytes are known to actively regulate T cell motility and thus are crucial for regulating T cell migration. The B7 co-stimulatory receptor family members CD28 and CTLA-4 are well known to positively and negatively regulate effector T cell motility respectively. However, their effect on motility and subsequently migration has not been specifically studied in regulatory T cells (Tregs). Tregs are a CD4+ T cell subset fundamental for maintaining immune homeostasis and their role in controlling autoimmunity has been well established through a variety of experimental animal models. Tregs differ from conventional T cells in their expression of CTLA-4. While conventional T cells express CTLA-4 only after activation, Tregs are known to express this negative co-stimulatory receptor constitutively. Additionally, Tregs display a distinct metabolic phenotype to that of conventional T cells. This thesis examines the impact of both co-stimulatory receptors on Treg migration while taking in account the consequences of the concomitant delivery of signals from both. The data in this study suggests that glycolysis, rather than lipid oxidation induced by CD28 promotes Treg migration through glycolytic enzymes including glucokinase, whose expression in T cells was previously unknown. In contrast, CTLA-4 inhibits CD28 induced Treg migration via inhibition of these glycolytic enzymes. The therapeutic implications of these results in the context of disease and transplantation are discussed. CD31, an IgG like molecule, is expressed on a number of leukocytes including lymphocytes. In T cells, CD31 inhibits activation by recruiting phosphatases through its cytoplasmic ITIM domains and has thus been described as a co-inhibitory receptor. The role of this co-receptor in the regulation of T cell migration is investigated in the last part of this thesis. Our observations suggest that CD31 selectively signals in activated T cells to regulate their migration in response to inflammatory chemokines, revealing an additional role of this receptor in regulating T cell-mediated inflammation.
Subjects/Keywords: Medicine; regulatory T cells; T cell migration
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Kishore, M. (2016). The role of co-stimulatory receptors in the regulation of regulatory T cell migration. (Doctoral Dissertation). Queen Mary, University of London. Retrieved from http://qmro.qmul.ac.uk/xmlui/handle/123456789/12869 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.775244
Chicago Manual of Style (16th Edition):
Kishore, Madhav. “The role of co-stimulatory receptors in the regulation of regulatory T cell migration.” 2016. Doctoral Dissertation, Queen Mary, University of London. Accessed March 04, 2021.
http://qmro.qmul.ac.uk/xmlui/handle/123456789/12869 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.775244.
MLA Handbook (7th Edition):
Kishore, Madhav. “The role of co-stimulatory receptors in the regulation of regulatory T cell migration.” 2016. Web. 04 Mar 2021.
Vancouver:
Kishore M. The role of co-stimulatory receptors in the regulation of regulatory T cell migration. [Internet] [Doctoral dissertation]. Queen Mary, University of London; 2016. [cited 2021 Mar 04].
Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/12869 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.775244.
Council of Science Editors:
Kishore M. The role of co-stimulatory receptors in the regulation of regulatory T cell migration. [Doctoral Dissertation]. Queen Mary, University of London; 2016. Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/12869 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.775244

University of Manchester
8.
Dookie, Rebecca.
Dissecting the molecular mechanisms of CD4+ T cell
exhaustion during malaria.
Degree: 2019, University of Manchester
URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:319548
► Malaria is a global life-threatening disease responsible for 400,000 deaths each year. Chronic infection with Plasmodium species drives CD4+ T cell exhaustion, which is characterised…
(more)
▼ Malaria is a global life-threatening disease
responsible for 400,000 deaths each year. Chronic infection with
Plasmodium species drives CD4+ T cell exhaustion, which is
characterised by the inability of effector CD4+ T cells to produce
effector cytokines, proliferate and increased T cell apoptosis. T
cell exhaustion significantly impairs parasite control during blood
stage malaria. However, the molecular mechanisms promoting CD4+ T
cell exhaustion during malaria are poorly understood. Using a model
antigen-specific CD4+ T cell system, we have shown that effector
CD4+ T cells rapidly become functionally exhausted during P.yoelii
infection. The degradation of the effector CD4+ T cell response
appeared to relate to the loss of MHC II-TCR signalling, as
blockade of MHC II signalling, post priming, did not exacerbate
effector T cell dysfunction and attrition during malaria. However,
apparent loss of MHC II activation during infection was not due to
alterations in CD4+ T cell compartmentalisation, or inability of
effector CD4+ T cells to interact with antigen presenting cells
(APC) during infection. Instead, we propose that negative signals
from co-inhibitory receptors subvert peptide MHC II-TCR signals in
effector CD4+ T cells, contributing to T cell exhaustion during
blood stage malaria. To further investigate the role of
co-inhibitory receptors in promoting CD4+ T cell exhaustion during
malaria, we administered antagonistic antibodies against TIGIT and
PD-L1. Dual blockade of TIGIT and PD-L1 significantly enhanced
parasite control, which correlated with an increased level of
systemic interferon gamma (IFNg) and an enhanced T follicular
helper response during infection. Surprisingly, however, dual
blockade of TIGIT and PD-L1 did not significantly improve effector
CD4+ T cell function. Thus, blockade of TIGIT and PD-1 signalling
pathways cannot prevent CD4+ T cell exhaustion during malaria. We
also investigated the synergistic role of Tim3 and PD-1 in
promoting CD4+ T cell exhaustion during malaria. Interestingly,
Tim3 was transiently expressed on effector CD4+ T cells and was
downregulated as T cell exhaustion was established during
infection. In agreement, co-blockade of Tim3 and PD-L1 failed to
improve CD4+ T cell functionality during P.yoelii infection,
suggesting that Tim3 does not contribute to CD4+ T cell exhaustion
during malaria. Collectively, this thesis has shown that effector
CD4+ T cell exhaustion is not associated with the inability of T
cells to form stable interactions with APC during infection, but
instead we propose that multiple immunoregulatory pathways act in
parallel to orchestrate T cell exhaustion during blood stage
malaria.
USB containing supplementary movies submitted in a
pocket on the inside back cover of the printed version of
thesis.
Advisors/Committee Members: MACDONALD, ANDREW AS, Couper, Kevin, Macdonald, Andrew.
Subjects/Keywords: CD4+ T cells; Malaria; T cell exhaustion
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Dookie, R. (2019). Dissecting the molecular mechanisms of CD4+ T cell
exhaustion during malaria. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:319548
Chicago Manual of Style (16th Edition):
Dookie, Rebecca. “Dissecting the molecular mechanisms of CD4+ T cell
exhaustion during malaria.” 2019. Doctoral Dissertation, University of Manchester. Accessed March 04, 2021.
http://www.manchester.ac.uk/escholar/uk-ac-man-scw:319548.
MLA Handbook (7th Edition):
Dookie, Rebecca. “Dissecting the molecular mechanisms of CD4+ T cell
exhaustion during malaria.” 2019. Web. 04 Mar 2021.
Vancouver:
Dookie R. Dissecting the molecular mechanisms of CD4+ T cell
exhaustion during malaria. [Internet] [Doctoral dissertation]. University of Manchester; 2019. [cited 2021 Mar 04].
Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:319548.
Council of Science Editors:
Dookie R. Dissecting the molecular mechanisms of CD4+ T cell
exhaustion during malaria. [Doctoral Dissertation]. University of Manchester; 2019. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:319548

Universiteit Utrecht
9.
Munting, L.P.
Reviewing seasonal child vaccination against influenza: An evaluation of the pros and cons.
Degree: 2015, Universiteit Utrecht
URL: http://dspace.library.uu.nl:8080/handle/1874/303162
► Influenza is an infectious, respiratory disease, which may cause symptoms in healthy individuals for several weeks. Serious complications or death may occur in the elderly…
(more)
▼ Influenza is an infectious, respiratory disease, which may cause symptoms in healthy individuals for several weeks. Serious complications or death may occur in the elderly and medically compromised patients. Vaccination is an effective means of preventing seasonal influenza infection. However, most countries do not vaccinate healthy individuals. Influenza infection of children is associated with additional aspects: children effectively spread influenza and both the child and its parents are affected. Should the Netherlands therefore include healthy children in the seasonal influenza vaccination target groups? The aim of this thesis is to provide a comprehensive review of the pros and cons of seasonal influenza vaccination in children. Influenza-specific
T cells play an important role in this evaluation.
Advisors/Committee Members: van Beek, Josine.
Subjects/Keywords: influenza; child vaccination; T cells
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Munting, L. P. (2015). Reviewing seasonal child vaccination against influenza: An evaluation of the pros and cons. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/303162
Chicago Manual of Style (16th Edition):
Munting, L P. “Reviewing seasonal child vaccination against influenza: An evaluation of the pros and cons.” 2015. Masters Thesis, Universiteit Utrecht. Accessed March 04, 2021.
http://dspace.library.uu.nl:8080/handle/1874/303162.
MLA Handbook (7th Edition):
Munting, L P. “Reviewing seasonal child vaccination against influenza: An evaluation of the pros and cons.” 2015. Web. 04 Mar 2021.
Vancouver:
Munting LP. Reviewing seasonal child vaccination against influenza: An evaluation of the pros and cons. [Internet] [Masters thesis]. Universiteit Utrecht; 2015. [cited 2021 Mar 04].
Available from: http://dspace.library.uu.nl:8080/handle/1874/303162.
Council of Science Editors:
Munting LP. Reviewing seasonal child vaccination against influenza: An evaluation of the pros and cons. [Masters Thesis]. Universiteit Utrecht; 2015. Available from: http://dspace.library.uu.nl:8080/handle/1874/303162

Tulane University
10.
Moss, Daniel.
Antigen Stability Influences Processing Efficiency and Immunogenicity of Pseudomonas Exotoxin Domain III and Ovalbumin.
Degree: 2020, Tulane University
URL: https://digitallibrary.tulane.edu/islandora/object/tulane:120437
► [email protected]
Effective adaptive immune responses depend on the presentation to CD4+ T cells antigen peptides bound to major histocompatibility complex class II proteins. The structure…
(more)
▼ [email protected]
Effective adaptive immune responses depend on the presentation to CD4+ T cells antigen peptides bound to major histocompatibility complex class II proteins. The structure of an antigen strongly influences its processing within the endolysosome and potentially controls the identity and abundance of peptides that are presented to T cells. The dissertation presented here sought to expand our understanding of how antigen structure and stability influence adaptive immune responses for two model antigens. Pseudomonas exotoxin A domain III (PE-III) functions as an ADP-ribosyltransferase with significant cellular toxicity and has been incorporated into a recombinant immunotoxin for the treatment of cancer. The bacterial component of the PE-III immunotoxin is highly immunogenic and generates neutralizing antibodies that render subsequent treatments ineffective. A group of six single-amino-acid substitutions in PE-III that were predicted to disrupt CD4+ T-cell epitopes have been shown to reduce antibody responses in mice. Here we demonstrate that only one of the substitutions, R494A, exhibits reduced folding stability and proteolytic resistance through the removal of a hydrogen bond. This destabilization significantly reduces its antibody immunogenicity while generating CD4+ T-cell epitopes that are indistinguishable from those of wildtype PE-III. PE-III specific B cells isolated from R494A-immunized animals contained fewer somatic mutations, which are associated with affinity maturation, and exhibited a weaker germinal-center gene signature, compared to B cells from wildtype-immunized animals. Chicken ovalbumin (cOVA) has been studied for decades primarily due to the robust genetic and molecular resources that are available for experimental investigations. cOVA is a member of the serpin superfamily of proteins that function as protease inhibitors, although cOVA does not exhibit this activity. As a serpin, cOVA possess a protease-sensitive reactive center loop that lies adjacent to the OT-II epitope. We took advantage of the previously described single-substitution-variant, OVA R339T, which can undergo the dramatic structural transition observed in serpins to study how changes in loop size and protein stability influences CD4+ T-cell priming in vivo. We observed that OVA R339T loop-insertion increases overall stability and protease resistance and significantly shortens the reactive center loop. This results in reduced CD4+ T-cell priming of the OT-II epitope in SJL mice. These findings have implications for the design of more effective vaccines for the treatment of infectious diseases and cancer as well as the development of more robust CD4+ T-cell epitope prediction tools.
1
Daniel Moss
Advisors/Committee Members: Landry, Samuel (Thesis advisor), School of Medicine Biomedical Sciences Graduate Program (Degree granting institution).
Subjects/Keywords: CD4+ T cells Antigen Processing
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Moss, D. (2020). Antigen Stability Influences Processing Efficiency and Immunogenicity of Pseudomonas Exotoxin Domain III and Ovalbumin. (Thesis). Tulane University. Retrieved from https://digitallibrary.tulane.edu/islandora/object/tulane:120437
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Moss, Daniel. “Antigen Stability Influences Processing Efficiency and Immunogenicity of Pseudomonas Exotoxin Domain III and Ovalbumin.” 2020. Thesis, Tulane University. Accessed March 04, 2021.
https://digitallibrary.tulane.edu/islandora/object/tulane:120437.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Moss, Daniel. “Antigen Stability Influences Processing Efficiency and Immunogenicity of Pseudomonas Exotoxin Domain III and Ovalbumin.” 2020. Web. 04 Mar 2021.
Vancouver:
Moss D. Antigen Stability Influences Processing Efficiency and Immunogenicity of Pseudomonas Exotoxin Domain III and Ovalbumin. [Internet] [Thesis]. Tulane University; 2020. [cited 2021 Mar 04].
Available from: https://digitallibrary.tulane.edu/islandora/object/tulane:120437.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Moss D. Antigen Stability Influences Processing Efficiency and Immunogenicity of Pseudomonas Exotoxin Domain III and Ovalbumin. [Thesis]. Tulane University; 2020. Available from: https://digitallibrary.tulane.edu/islandora/object/tulane:120437
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Alberta
11.
Hockley, Deanna L.
Co-stimulator contributions in CD8+ T cell
differentiation.
Degree: PhD, Department of Medical Microbiology and
Immunology, 2012, University of Alberta
URL: https://era.library.ualberta.ca/files/f4752h04p
► The adaptive immune response against intracellular pathogens is largely mediated by CD8+ T lymphocytes. The clonal expansion and expression of cytolytic and immune stimulatory proteins…
(more)
▼ The adaptive immune response against intracellular
pathogens is largely mediated by CD8+ T lymphocytes. The clonal
expansion and expression of cytolytic and immune stimulatory
proteins by CD8+ T cells is responsible for their protective immune
function. Prior to exhibiting effector activity, CD8+ T cells exist
in a naïve state and require three stimulatory signals for their
optimal activation including the recognition of antigen,
co-stimulator ligand engagement, and the presence of
pro-inflammatory cytokines. When these activation requirements are
met, CD8+ T cells undergo a well described series of events
including clonal expansion, cellular contraction, memory
generation, and memory maintenance. The memory CD8+ T cell
population generated can survive for the life-time of the host, and
provides more rapid and robust protection upon re-infection then
their naïve precursors. While some factors that induce this
sequence of events have been identified, the role of co-stimulation
remains relatively undefined. This is due to the large number of
co-stimulator receptors expressed by CD8+ T cells that may be
ligated individually and/or in combination, to instruct the
development of specific effector and memory CD8+ T cell phenotypes.
Using a bead-based ligand presentation system, I investigated the
role of co-stimulation in directing naïve CD8+ T cell activation,
and the generation of T cell populations with distinct effector and
memory fates. I identified ICAM-1 as the stimulatory molecule best
able to induce naïve CD8+ T cell proliferation and expression of
the effector molecule granzyme B, while co-stimulation through CD28
was required to induce IFN-γ. When provided in combination however,
B7.1 and ICAM-1 co-stimulation generated CD8+ T cells which were
highly cytolytic and expressed high amounts of IFN-γ. These cells
also exhibited enhanced survival once activated, with sustained
expression of anti-apoptotic proteins and secretion of high amounts
of IL-2, resulting in these cells exhibiting a terminal effector
phenotype. While other co-stimulator combinations also enhanced
CD8+ T cell survival to some degree, their ability to sustain high
expression of IL-2 was limited. This translated into less potent
effector responses and preferential memory precursor development
based on transcription factor expression.
Subjects/Keywords: Immunology; T cells; Co-stimulation
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Hockley, D. L. (2012). Co-stimulator contributions in CD8+ T cell
differentiation. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/f4752h04p
Chicago Manual of Style (16th Edition):
Hockley, Deanna L. “Co-stimulator contributions in CD8+ T cell
differentiation.” 2012. Doctoral Dissertation, University of Alberta. Accessed March 04, 2021.
https://era.library.ualberta.ca/files/f4752h04p.
MLA Handbook (7th Edition):
Hockley, Deanna L. “Co-stimulator contributions in CD8+ T cell
differentiation.” 2012. Web. 04 Mar 2021.
Vancouver:
Hockley DL. Co-stimulator contributions in CD8+ T cell
differentiation. [Internet] [Doctoral dissertation]. University of Alberta; 2012. [cited 2021 Mar 04].
Available from: https://era.library.ualberta.ca/files/f4752h04p.
Council of Science Editors:
Hockley DL. Co-stimulator contributions in CD8+ T cell
differentiation. [Doctoral Dissertation]. University of Alberta; 2012. Available from: https://era.library.ualberta.ca/files/f4752h04p

University of Alberta
12.
He, Jinshu.
Regulation of FasL expression and trafficking in cytotoxic T
lymphocytes.
Degree: PhD, Department of Medical Microbiology and
Immunology, 2009, University of Alberta
URL: https://era.library.ualberta.ca/files/4x51hj17q
► Cytotoxic T lymphocytes (CTL) are differentiated CD8+ T cells that eliminate virally infected cells and tumor cells. CTL lyse target cells by at least two…
(more)
▼ Cytotoxic T lymphocytes (CTL) are differentiated CD8+
T cells that eliminate virally infected cells and tumor cells. CTL
lyse target cells by at least two distinct mechanisms:
degranulation of cytolytic molecules and cell surface expression of
Fas ligand (FasL), which induces apoptosis of Fas-expressing target
cells. In addition to their defense function, these two cytolytic
mechanisms also play crucial roles in homeostatic regulation and
contribute to pathogenesis in many different model systems. To
fully exploit killer cells in tumor and virus elimination, or
dampen the immune response in, for example, autoimmune diseases, it
is essential to understand the mechanisms that CTL employ to
destroy target cells. In contrast to the well-characterized
degranulation mechanism, the regulation of FasL expression on the
CTL cell surface remains elusive and even controversial. The
prevailing model at the time I initiated my studies was that FasL
is stored in cytolytic granules and that FasL cell surface
expression would be subject to the same controls as degranulation.
In this thesis, I revealed for the first time that there are two
waves of FasL cell surface expression upon target cell engagement,
which are differentially regulated by TCR signaling and perform
distinct roles in CTL mediated responses. I demonstrated that CTL
degranulation and FasL lytic mechanisms are fully independent with
respect to stored component localization and regulation. Finally,
based on cell fractionation and imaging studies, I suggested that
FasL is stored in a recycling endosome associated compartment,
which is located in a special niche between the ER and mitochondria
and uses a novel microtubule-independent secretory mechanism to
translocate to the cell surface. Together, these findings provide
important insight into the regulation and role of FasL in CTL
mediated responses.
Subjects/Keywords: cytotoxicity; T cells; Fas ligand
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
He, J. (2009). Regulation of FasL expression and trafficking in cytotoxic T
lymphocytes. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/4x51hj17q
Chicago Manual of Style (16th Edition):
He, Jinshu. “Regulation of FasL expression and trafficking in cytotoxic T
lymphocytes.” 2009. Doctoral Dissertation, University of Alberta. Accessed March 04, 2021.
https://era.library.ualberta.ca/files/4x51hj17q.
MLA Handbook (7th Edition):
He, Jinshu. “Regulation of FasL expression and trafficking in cytotoxic T
lymphocytes.” 2009. Web. 04 Mar 2021.
Vancouver:
He J. Regulation of FasL expression and trafficking in cytotoxic T
lymphocytes. [Internet] [Doctoral dissertation]. University of Alberta; 2009. [cited 2021 Mar 04].
Available from: https://era.library.ualberta.ca/files/4x51hj17q.
Council of Science Editors:
He J. Regulation of FasL expression and trafficking in cytotoxic T
lymphocytes. [Doctoral Dissertation]. University of Alberta; 2009. Available from: https://era.library.ualberta.ca/files/4x51hj17q
13.
佐伯, 晃一.
THEORETICAL STUDIES OF SELF-TOLERANCE : REGULATORY T CELLS AND ANERGY : 自己寛容に関する理論的研究 : 制御性T細胞とアナジーについて.
Degree: 博士(理学), 2013, Kyushu University / 九州大学
URL: http://hdl.handle.net/2324/21712
;
http://dx.doi.org/10.15017/21712
自己寛容とは免疫システムが自分の体に対して反応を示さない状態のことである。これは生物が生まれながらに持っている性質ではなく、成立にはその為のメカニズムが必要である。例えば、獲得免疫系を担うリンパ球はランダムに生成された受容体を用いて抗原の認識を行うため、自分の体由来の抗原を認識するリンパ球も作られる。そのため成熟前に受容体をチェックし、自己抗原を認識するものは排除する(負の選択)機構が存在する。しかしながら、このチェック機構だけでは不十分であり、リンパ球の成熟後に末梢において自己寛容を保証するメカニズムがあることが知られている。自己寛容の破綻は自己免疫疾患につながるため、メカニズムの理解は医学的な観点からも注目を集めている。本論文では、自己寛容の成立に関わっている二つの機構、制御性T細胞とアナジーに着目しそれらの意義ついて数理モデルを用いて議論した。二つの機構は常に有益となるわけではなく、幾つかの条件下で有利に働くことが分かった。
Advisors/Committee Members: 巌佐, 庸.
Subjects/Keywords: self-tolerance; regulatory T cells
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
佐伯, . (2013). THEORETICAL STUDIES OF SELF-TOLERANCE : REGULATORY T CELLS AND ANERGY : 自己寛容に関する理論的研究 : 制御性T細胞とアナジーについて. (Thesis). Kyushu University / 九州大学. Retrieved from http://hdl.handle.net/2324/21712 ; http://dx.doi.org/10.15017/21712
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
佐伯, 晃一. “THEORETICAL STUDIES OF SELF-TOLERANCE : REGULATORY T CELLS AND ANERGY : 自己寛容に関する理論的研究 : 制御性T細胞とアナジーについて.” 2013. Thesis, Kyushu University / 九州大学. Accessed March 04, 2021.
http://hdl.handle.net/2324/21712 ; http://dx.doi.org/10.15017/21712.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
佐伯, 晃一. “THEORETICAL STUDIES OF SELF-TOLERANCE : REGULATORY T CELLS AND ANERGY : 自己寛容に関する理論的研究 : 制御性T細胞とアナジーについて.” 2013. Web. 04 Mar 2021.
Vancouver:
佐伯 . THEORETICAL STUDIES OF SELF-TOLERANCE : REGULATORY T CELLS AND ANERGY : 自己寛容に関する理論的研究 : 制御性T細胞とアナジーについて. [Internet] [Thesis]. Kyushu University / 九州大学; 2013. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/2324/21712 ; http://dx.doi.org/10.15017/21712.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
佐伯 . THEORETICAL STUDIES OF SELF-TOLERANCE : REGULATORY T CELLS AND ANERGY : 自己寛容に関する理論的研究 : 制御性T細胞とアナジーについて. [Thesis]. Kyushu University / 九州大学; 2013. Available from: http://hdl.handle.net/2324/21712 ; http://dx.doi.org/10.15017/21712
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Oregon State University
14.
Maxwell, Joseph R.
The role of costimulation and adjuvants in the development of T cell effector and memory responses.
Degree: PhD, Microbiology, 2001, Oregon State University
URL: http://hdl.handle.net/1957/32495
► T cells are one of the key cells in the immune system. Although they are not the first line of defense against a pathogen, their…
(more)
▼ T cells are one of the key
cells in the immune system. Although they are
not the first line of defense against a pathogen, their functions can greatly enhance
the phagocytosis and destruction of pathogens as well as the development of
antibody responses. Furthermore, even when responding
T cells have facilitated
the clearance of the pathogen, they can avoid death to become long-lived
cells that
"remember" encountering the pathogen for years afterward. This long-term
memory allows subsequent immune responses to improve with each exposure,
ultimately preventing disease upon reinfection. The activation of these
T cells
depends on specific recognition of antigen along with a costimulatory signal. This
activation process is well studied, but not completely understood. Additionally, the
mechanism behind memory
T cell development is still very much unknown. In the
work presented in this thesis, delivery of costimulatory signals via CD4O and 0X40
were studied using an in vivo superantigen (SAg) model of
T cell stimulation. In
the context of this two-signal (SAg + costimulation) model, both CD4O and OX40
could deliver signals that enhanced SAg-reactive
T cell clonal expansion, but they
could only partially prevent
T cell death. Coadministration of the inflammatory
agent lipopolysaccharide (LPS), however, could keep increased responder
T cell
populations alive for at least two months. Interestingly, this three-signal (SAg +
costimulation + LPS) induced survival was not dependent on proinflammatory
cytokines or activation of the transcription factor NF-KB, but was sensitive to the
immunosuppressant cyclosporin A (CsA). The mode of action of CsA may point to
the mechanism driving long-term
T cell survival. Additionally, examination of
early time points after three-signal stimulation suggested more clues to the
mechanism of survival induction. The cytokines IL-2 and TNF-α seem to be
involved early on, but for now, little is known about their complete role. Thus, the
goal of this work was to investigate the costimulatory and adjuvant-mediated
signals required for memory
T cell development. Ultimately, an understanding of
how memory
T cells can be generated could be used to enhance vaccine efficacy or
shut off autoimmune conditions.
Advisors/Committee Members: Vella, Anthony T. (advisor).
Subjects/Keywords: T cells
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Maxwell, J. R. (2001). The role of costimulation and adjuvants in the development of T cell effector and memory responses. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/32495
Chicago Manual of Style (16th Edition):
Maxwell, Joseph R. “The role of costimulation and adjuvants in the development of T cell effector and memory responses.” 2001. Doctoral Dissertation, Oregon State University. Accessed March 04, 2021.
http://hdl.handle.net/1957/32495.
MLA Handbook (7th Edition):
Maxwell, Joseph R. “The role of costimulation and adjuvants in the development of T cell effector and memory responses.” 2001. Web. 04 Mar 2021.
Vancouver:
Maxwell JR. The role of costimulation and adjuvants in the development of T cell effector and memory responses. [Internet] [Doctoral dissertation]. Oregon State University; 2001. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/1957/32495.
Council of Science Editors:
Maxwell JR. The role of costimulation and adjuvants in the development of T cell effector and memory responses. [Doctoral Dissertation]. Oregon State University; 2001. Available from: http://hdl.handle.net/1957/32495

University of Manchester
15.
Davies, Sian.
T Cell Phenotypes in Upper Gastrointestinal
Cancers.
Degree: 2016, University of Manchester
URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:300583
► AbstractBackground: Upper gastrointestinal adenocarcinomas are increasing in prevalence, particularly oesophageal cancer where the incidence rates have increased by over 65% in the last 30 years.…
(more)
▼ AbstractBackground: Upper gastrointestinal
adenocarcinomas are increasing in prevalence, particularly
oesophageal cancer where the incidence rates have increased by over
65% in the last 30 years. Both adenocarcinomas are associated with
very poor outcomes; the 5 year survival rate for oesophageal cancer
being only 15% and gastric cancer 19%. There has been limited
research into the role of the immune system in the development and
treatment of upper gastrointestinal adenocarcinomas. Some studies
have suggested that certain
T helper subsets, including Th17 and
Th22
cells, may play a role in these cancers and could therefore be
a potential area of further study. However the classification of
these cell types has altered over time in part due to the increased
availability of marker–specific antibodies and increased power of
multi-colour flow cytometry technology. Thus, the limited ability
to clearly detect specific
T cell subsets in earlier studies may
have contributed to the contradictory roles predicted for these
T
helper subsets
cells in the development of upper gastrointestinal
malignancy. Aims: This project focuses on developing multi-colour
flow cytometry panels that can accurately identify the diversity of
T helper cell phenotypes and use these techniques to further
explore the role these
cells may have in the development and
disease process of upper gastrointestinal adenocarcinomas.Methods:
Blood samples from healthy donors and patients with either gastric
adenocarcinoma or oesophageal adenocarcinoma would be collected and
matched peripheral blood mononuclear
cells (PBMC) isolated.
Experiments were performed to develop an optimized flow cytometry
panel that could identify the subtype populations of CD4
cells Th17
and Th22 by varying the duration of activation and the freeze /
thawing of the PBMCs. Alongside this process, a flow cytometry
technique was developed to optimize the identification of these
populations. Once this methodological process was optimised,
healthy donor PBMCs and gastric or oesophageal cancer PBMCs were
analysed to determine the relative frequency of Th17 and Th22
cells
within the different patient and healthy donor cellular
populations. Results: The optimal activation period to
identification of Th17 and Th22
cells was 16 hours. Moreover,
freeze / thawing had minimal impact on the ability to identify
these populations thereby facilitating the batched analysis with
improved consistency in sample analysis. A flow cytometry panel of
10 flourochromes was also designed and optimised to more accurately
improve identification of Th17 and Th22 by their cytokine profiles
CD3+CD4+IL17+IL10-INF?- and CD3+CD4+IL22+IL17-TNF?+ respectively.
To also identify the possible plastic nature of Th17
cells, further
populations were defined by their cytokine profiles Th17/Treg
(CD3+CD4+IL-17+IL-10+INF?-) and Th17/Th1
(CD3+CD4+IL-17+IL-10-INF?+). Analyses of these populations in
healthy donor PBMCs found a significant positive correlation
between the relative frequency of Th17 and Th22
cells, Th17/Th1 and
Th22…
Advisors/Committee Members: MANSOOR, ABDUL AW, GALLOWAY, SIMON S, Gilham, David, Mansoor, Abdul, Galloway, Simon.
Subjects/Keywords: T Cells; Upper GI Cancers
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APA (6th Edition):
Davies, S. (2016). T Cell Phenotypes in Upper Gastrointestinal
Cancers. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:300583
Chicago Manual of Style (16th Edition):
Davies, Sian. “T Cell Phenotypes in Upper Gastrointestinal
Cancers.” 2016. Doctoral Dissertation, University of Manchester. Accessed March 04, 2021.
http://www.manchester.ac.uk/escholar/uk-ac-man-scw:300583.
MLA Handbook (7th Edition):
Davies, Sian. “T Cell Phenotypes in Upper Gastrointestinal
Cancers.” 2016. Web. 04 Mar 2021.
Vancouver:
Davies S. T Cell Phenotypes in Upper Gastrointestinal
Cancers. [Internet] [Doctoral dissertation]. University of Manchester; 2016. [cited 2021 Mar 04].
Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:300583.
Council of Science Editors:
Davies S. T Cell Phenotypes in Upper Gastrointestinal
Cancers. [Doctoral Dissertation]. University of Manchester; 2016. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:300583

Cornell University
16.
Carter, Chavez.
Role Of Itk In Th17 Mediated Inflammation Model Hypersensitivity Pneumonitis.
Degree: PhD, Immunology, 2015, Cornell University
URL: http://hdl.handle.net/1813/41075
► Hypersensitivity Pneumonitis (HP) is a lung disease caused by repeated inhalation of environmental antigens leading to inflammation, tissue scarring, and some loss of lung function.…
(more)
▼ Hypersensitivity Pneumonitis (HP) is a lung disease caused by repeated inhalation of environmental antigens leading to inflammation, tissue scarring, and some loss of lung function. This pathology is believed to be due to the increased IL-17A, a cytokine secreted predominantly by a subset of
T cells, Th17
cells, that induces recruitment of inflammatory
cells such as neutrophils and leads to pathology in this disease. The thermophile Sacharopolyspora rectivigula (SR) causes HP in humans, and we have used a murine model of HP, exposure to SR, to study the molecular mechanism of disease development. Using novel IL-17A-GFP reporter mice, our preliminary data suggests that the high levels of IL-17A induced in response to SR are produced in part by CD4+
T cells and not by neutrophils. The Tec family tyrosine kinase Itk is a pharmaceutical target and regulates
T cell activation and cytokine production, including Th2 cytokines and IL-17A in conventional Th17
cells. Mice lacking Itk are therefore resistant to developing Th2 cytokine driven allergic lung inflammation. However our experiments indicate that mice lacking Itk develop HP. Histology from these mice indicates an increase in inflammatory
cells in lung airways as well as deterioration of lung tissue architecture. Mice lacking Itk also have significant levels of IL-17A mRNA expression in the lung, and an increase in the number of CD4+ IL-17A producing
cells. Furthermore, the lack of Itk signaling led to the absence of IL-17A producing [gamma][delta]
T cells in the early stage of HP, which recover over the later stage of disease. This phenomenon directly coincides with the emergence of IL-17A producing CD4+[gamma][delta]
T cells in the lungs of Itk-/- mice exposed to SR. We conclude that Itk regulated signals are not critical for the production of IL-17A in response to SR, and Itk may therefore differentially regulate the production of IL-17A in different types of
T cells. We also show that the inhibition of Itk kinase signaling can be inhibited by targeting allele sensitive Itkas. The block in kinase activity leads to decrease response of response in the BAL and lungs. We investigate the relationship between Th17 cell and
T regulatory
T cells in an IL-17A driven disease as it relates to Itk signaling. We find that Itk signaling is not altering the proportion or numbers of
T regulatory
cells. Additionally, we show that iNKT
cells are a possible source of IL-17A and this primarily independent of Itk signal as well. Lastly, we investigate the role of IL4Ra signaling and indirectly innate memory phenotype (IMP)
cells in HP. Our data shows IL-4 signaling as well as IMP
cells play a protective role in the BAL during HP. Furthermore, IL-4Ra and IMP
cells are partially responsible for the number of CD4+
T cells seen in HP, which is independent of Itk-/- mice ability to make IL-17A cytokine in SR induced HP. SR induced HP. ! Together, you data show Itk mediate differential immune responses in
Advisors/Committee Members: August,Avery (chair), Bynoe,Margaret S. (committee member), Rudd,Brian D (committee member).
Subjects/Keywords: Itk; Hypersensitivity Pneumonitis; T cells
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Carter, C. (2015). Role Of Itk In Th17 Mediated Inflammation Model Hypersensitivity Pneumonitis. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/41075
Chicago Manual of Style (16th Edition):
Carter, Chavez. “Role Of Itk In Th17 Mediated Inflammation Model Hypersensitivity Pneumonitis.” 2015. Doctoral Dissertation, Cornell University. Accessed March 04, 2021.
http://hdl.handle.net/1813/41075.
MLA Handbook (7th Edition):
Carter, Chavez. “Role Of Itk In Th17 Mediated Inflammation Model Hypersensitivity Pneumonitis.” 2015. Web. 04 Mar 2021.
Vancouver:
Carter C. Role Of Itk In Th17 Mediated Inflammation Model Hypersensitivity Pneumonitis. [Internet] [Doctoral dissertation]. Cornell University; 2015. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/1813/41075.
Council of Science Editors:
Carter C. Role Of Itk In Th17 Mediated Inflammation Model Hypersensitivity Pneumonitis. [Doctoral Dissertation]. Cornell University; 2015. Available from: http://hdl.handle.net/1813/41075

University of Otago
17.
Czepluch, Wenzel.
Factors mediating successful oral vaccination with lipid-encapsulated Mycobacterium bovis BCG
.
Degree: 2012, University of Otago
URL: http://hdl.handle.net/10523/2086
► During the course of this thesis factors mediating successful oral vaccination with lipidencapsulated Mycobacterium bovis BCG were examined. Mice were fed 2x10E07 CFU BCG encapsulated…
(more)
▼ During the course of this thesis factors mediating successful oral vaccination with lipidencapsulated Mycobacterium bovis BCG were examined. Mice were fed 2x10E07 CFU BCG encapsulated into a lipid matrix to prevent destruction by the gastrointestinal tract and to allow passage through the gut epithelia. In order to trace the vaccine following oral
vaccination, mice were sacrificed at various time points ranging from 6 hours to 8 weeks post vaccination, and macerated lymphatic and non-lymphatic organs plated on solid agar. Initially, BCG was distributed widely in lymphatic and non-lymphatic organs, however, BCG was cleared quickly from most organs and formed small populations of less than 500 CFU/mouse in the mesenteric and cervical lymph nodes, as well as the Peyer’s patches 8 weeks post vaccination. Immuno-histochemistry and confocal microscopy, showed that BCG was absent from the follicles, but instead resided in the
T cell containing intra-follicular areas. Very rarely BCG was associated with small CD11b+
cells that did not resemble typical macrophages and lacked peroxidase activity. Instead the majority of BCG could be found forming extracellular groups of 1-4 rods. This was confirmed using cell sorting of leukocytes isolated from alimentary tract lymphatics of orally vaccinated mice and only showed a minority of BCG to be associated with CD11c+
cells. Therefore, BCG is absent from typical antigen presenting
cells, but instead might reside in CD11c+CD11b+ myeloid DC.
Additionally, Ziehl-Neelsen staining revealed groups of intracellular coccoid forms of BCG. These were located toward the subcapsular space of draining lymph nodes where they were associated with sub-capsular macrophages. Interestingly, cocci proved to be non-platable using solid agar but instead required resuscitation in liquid media and therefore might resemble a form of dormancy. The presence of extracellular rods and intracellular cocci in on-professional antigen presenting
cells might highlight the importance of secreted factors as an antigen source promoting successful activation of the immune system.
Following oral vaccination, IFN-γ producing
cells almost exclusively resided in the spleen. In order to characterize these
cells, splenocytes of orally vaccinated mice were isolated 6 weeks post vaccination on the basis of surface marker expression using fluorescence activated cell sorting (FACS).
Antigen-specific release of IFN-γ was monitored using ELISA and ELISpot assays and IFN-γ producing
T cells were characterized as
T effector memory
cells expressing CD44,
but not CD62L and lacked the expression of mucosal homing markers such as CD103 or α4β7. In addition, Lincoplex assays revealed the production of IL-17 by splenocytes.
These did not express CD4+ but rather the γδ
T cell eceptor.
Together these results show that antigen reservoirs of BCG present in the draining lymphatics contain small numbers
of typical filamentous BCG. A larger population of coccoid forms leaves open the possibility that coccoid forms are a major source of antigen…
Advisors/Committee Members: McLellan, Alexander Donald (advisor).
Subjects/Keywords: BCG vaccination;
T cells DC
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Czepluch, W. (2012). Factors mediating successful oral vaccination with lipid-encapsulated Mycobacterium bovis BCG
. (Doctoral Dissertation). University of Otago. Retrieved from http://hdl.handle.net/10523/2086
Chicago Manual of Style (16th Edition):
Czepluch, Wenzel. “Factors mediating successful oral vaccination with lipid-encapsulated Mycobacterium bovis BCG
.” 2012. Doctoral Dissertation, University of Otago. Accessed March 04, 2021.
http://hdl.handle.net/10523/2086.
MLA Handbook (7th Edition):
Czepluch, Wenzel. “Factors mediating successful oral vaccination with lipid-encapsulated Mycobacterium bovis BCG
.” 2012. Web. 04 Mar 2021.
Vancouver:
Czepluch W. Factors mediating successful oral vaccination with lipid-encapsulated Mycobacterium bovis BCG
. [Internet] [Doctoral dissertation]. University of Otago; 2012. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/10523/2086.
Council of Science Editors:
Czepluch W. Factors mediating successful oral vaccination with lipid-encapsulated Mycobacterium bovis BCG
. [Doctoral Dissertation]. University of Otago; 2012. Available from: http://hdl.handle.net/10523/2086

University of Cambridge
18.
Alam, Rafeah.
T cell phenotyping of a mouse model of Activated PI3Kdelta syndrome.
Degree: PhD, 2019, University of Cambridge
URL: https://www.repository.cam.ac.uk/handle/1810/293595
► Activated PI3Kdelta Syndrome (APDS) is immunodeficiency caused by a heterozygous gain-of-function mutation (E1021K) in the PIK3CD gene, encoding for the p110delta catalytic subunit of phosphoinositide…
(more)
▼ Activated PI3Kdelta Syndrome (APDS) is immunodeficiency caused by a heterozygous gain-of-function mutation (E1021K) in the PIK3CD gene, encoding for the p110delta catalytic subunit of phosphoinositide 3-kinase (PI3K). APDS patients are lymphopenic, suffer from sinopulmonary infections and from increased susceptibility to bacterial and herpes group virus infections. Following T cell receptor (TCR) stimulation, T cells from these patients undergo increased activation induced cell death, which can be reversed by selective PI3Kdelta inhibitors. I used a new conditional knock-in mouse (T-p110delta E1020K) in order to investigate the effect of hyperactive p110delta on T cell function. Hyperactivation of p110delta led to increased PIP3 and pAKT levels following TCR stimulation that was reduced using a selective p110delta inhibitor. Following in vitro TCR stimulation, T cells proliferated normally but showed increased apoptosis that was reversed by a p110delta specific inhibitor. Despite enhanced apoptosis, CD8+ T cells displayed enhanced activation that was associated with increased levels of cytokines and granzyme B. CD4+ T cells with hyperactive p110delta produced increased Th1, Th2, Th17 and Tfh cytokines but showed reduced Treg differentiation in vitro. Conditional T-p110delta E1020K mice have reduced Tregs in the thymus but increased peripheral Tregs. These mice also have increased numbers of T follicular helper cells and germinal centre (GC) B cells upon immunisation with a T cell dependent antigen (NP-KLH). Reduced antigen specific IgG1+ cells within GC B cells was detected in mice harbouring hyperactive p110delta mutation in B cells, implying that the antibody deficiencies observed in APDS patients is due to an intrinsic defect within B cells rather than limited help from T cells.
T-p110delta E1020K mice mounted normal primary responses to acute infections .However adoptive transfer of ovalbumin-specific T cell receptor transgenic CD8 T cells (OT1) revealed an intrinsic defect in the primary expansion of CD8+ T cells with hyperactive p110delta. This defect in primary expansion was found to be rescued in the presence of wild type OT1 cells. Following infection with acute pathogens, CD8+ T cells with hyperactive p110delta displayed normal to increased effector function with phenotypically reduced memory cells as indicated by reduced memory precursor effectors cells (MPECs). In contrast, following chronic infection, T-p110delta E1020K displayed increased signs of T cell exhaustion that is also characteristic of APDS patients as they suffer from chronic herpes virus infections. This set of work therefore shows that the mouse model recapitulates key aspects of APDS patients and give insights into the role of p110delta signaling in different T cell subsets influenced by hyperactive p110delta activity. Further, in depth analysis of proteomics and gene array data of in vitro stimulated T cells generated during this study, can provide a better understanding of the mechanisms behind the T cell phenotype observed.
Subjects/Keywords: APDS; PI3K; T cells
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Alam, R. (2019). T cell phenotyping of a mouse model of Activated PI3Kdelta syndrome. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/293595
Chicago Manual of Style (16th Edition):
Alam, Rafeah. “T cell phenotyping of a mouse model of Activated PI3Kdelta syndrome.” 2019. Doctoral Dissertation, University of Cambridge. Accessed March 04, 2021.
https://www.repository.cam.ac.uk/handle/1810/293595.
MLA Handbook (7th Edition):
Alam, Rafeah. “T cell phenotyping of a mouse model of Activated PI3Kdelta syndrome.” 2019. Web. 04 Mar 2021.
Vancouver:
Alam R. T cell phenotyping of a mouse model of Activated PI3Kdelta syndrome. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Mar 04].
Available from: https://www.repository.cam.ac.uk/handle/1810/293595.
Council of Science Editors:
Alam R. T cell phenotyping of a mouse model of Activated PI3Kdelta syndrome. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/293595

University of Cambridge
19.
Strege, Katharina.
Identifying regulators of cytotoxic T cell function through molecular and genetic screening.
Degree: PhD, 2019, University of Cambridge
URL: https://www.repository.cam.ac.uk/handle/1810/293498https://www.repository.cam.ac.uk/bitstream/1810/293498/2/AppendixB.csv
► Cytotoxic T lymphocytes (CTL) are crucial components of the adaptive immune system that kill infected and tumourigenic cells. CTL killing requires focused secretion of cytotoxic…
(more)
▼ Cytotoxic T lymphocytes (CTL) are crucial components of the adaptive immune system that kill infected and tumourigenic cells. CTL killing requires focused secretion of cytotoxic compounds from lytic granules. This process is known as degranulation. In this study, I aimed to establish the CRISPR-Cas9 gene editing technology in primary T cells and to optimise screening approaches to identify regulators of CTL killing.
The first half of the thesis focuses on primary mouse CTL. The CRISPR technology was successfully optimised in CTL using Cas9-ribonucleoprotein complexes resulting in efficient CRISPR-mediated loss of target proteins. Genes encoding known mediators of CTL cytotoxicity, \it{Rab27a}, \it{Munc13-4} and \it{Prf1}, were targeted using CRISPR. The resulting samples were used to establish a flow cytometry-based assay that simultaneously measures CTL degranulation and target cell death.
This assay enabled me to screen for mediators of CTL killing, while providing mechanistic insight by detecting degranulation. The screen was informed by a transcriptomic study that compared naive and effector CD8 T cells. 1803 significantly upregulated differentially expressed genes [log2(fold change)>2] were identified. Functional annotation analysis and literature research were used to select genes for the targeted CRISPR screen, which highlighted the importance of HIF-1α and NFIL3 in CTL killing.
The second half of the thesis focuses on primary human CTL. The combined degranulation and killing assay was further validated using patient-derived CTL, indicating its potential as a diagnostic test. I showed that the assay is suitable for mid-sized screens using a library of 64 compounds targeting the NF-κB signalling pathway. Further opportunities for increasing the scale of this screening technique are discussed.
Finally, I successfully tested CRISPR using Cas9-ribonucleoprotein complexes in the human system. Additionally, stable Cas9 expression through lentiviral transduction was explored in primary CTL and related cell lines. This has the potential to allow selection of cells expressing the CRISPR machinery, providing a cleaner experimental system and the possibility of large-scale screening approaches.
In summary, the techniques established in this thesis will be valuable for studying the genetics underlying CTL killing and the combined degranulation and killing assay furthermore shows great potential for diagnostic purposes.
Subjects/Keywords: Cytotoxic T cells; CRISPR; screening
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Strege, K. (2019). Identifying regulators of cytotoxic T cell function through molecular and genetic screening. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/293498https://www.repository.cam.ac.uk/bitstream/1810/293498/2/AppendixB.csv
Chicago Manual of Style (16th Edition):
Strege, Katharina. “Identifying regulators of cytotoxic T cell function through molecular and genetic screening.” 2019. Doctoral Dissertation, University of Cambridge. Accessed March 04, 2021.
https://www.repository.cam.ac.uk/handle/1810/293498https://www.repository.cam.ac.uk/bitstream/1810/293498/2/AppendixB.csv.
MLA Handbook (7th Edition):
Strege, Katharina. “Identifying regulators of cytotoxic T cell function through molecular and genetic screening.” 2019. Web. 04 Mar 2021.
Vancouver:
Strege K. Identifying regulators of cytotoxic T cell function through molecular and genetic screening. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Mar 04].
Available from: https://www.repository.cam.ac.uk/handle/1810/293498https://www.repository.cam.ac.uk/bitstream/1810/293498/2/AppendixB.csv.
Council of Science Editors:
Strege K. Identifying regulators of cytotoxic T cell function through molecular and genetic screening. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/293498https://www.repository.cam.ac.uk/bitstream/1810/293498/2/AppendixB.csv

Columbia University
20.
Cvetkovski, Filip.
Transcriptional control of tissue-resident memory T cell generation.
Degree: 2019, Columbia University
URL: https://doi.org/10.7916/d8-n16c-b343
► Tissue-resident memory T cells (TRM) are a non-circulating subset of memory that are maintained at sites of pathogen entry and mediate optimal protection against reinfection.…
(more)
▼ Tissue-resident memory T cells (TRM) are a non-circulating subset of memory that are maintained at sites of pathogen entry and mediate optimal protection against reinfection. Lung TRM can be generated in response to respiratory infection or vaccination, however, the molecular pathways involved in CD4+TRM establishment have not been defined. Here, we performed transcriptional profiling of influenza-specific lung CD4+TRM following influenza infection to identify pathways implicated in CD4+TRM generation and homeostasis. Lung CD4+TRM displayed a unique transcriptional profile distinct from spleen memory, including up-regulation of a gene network induced by the transcription factor IRF4, a known regulator of effector T cell differentiation. In addition, the gene expression profile of lung CD4+TRM was enriched in gene sets previously described in tissue-resident regulatory T cells. Up-regulation of immunomodulatory molecules such as CTLA-4, PD-1, and ICOS, suggested a potential regulatory role for CD4+TRM in tissues. Using loss-of-function genetic experiments in mice, we demonstrate that IRF4 is required for the generation of lung-localized pathogen-specific effector CD4+T cells during acute influenza infection. Influenza-specific IRF4−/− T cells failed to fully express CD44, and maintained high levels of CD62L compared to wild type, suggesting a defect in complete differentiation into lung-tropic effector T cells. This finding identifies IRF4 as an important regulator of CD4+TRM generation in response to respiratory infection.
Furthermore, comparing whole transcriptome profiling of mouse and human lung memory T cell subsets, we define a lung CD4+TRM gene signature common to mice and humans. IRF4 protein was specifically up-regulated in lung CD4+TRM but not in circulating memory subsets, in both humans and mice previously infected with influenza. This result suggest that high expression of IRF4 contributes to a cross-species conserved molecular pathway of long term maintenance of CD4+TRM in the lung. Overall, our findings confirm lung CD4+TRM as a unique memory T cell subset regulated by tissue-specific transcription factors. These results have important implications in focusing future studies of tissue resident memory T cells to factors with translational potential. Importantly, by determining the lung CD4+TRM gene signature common to mice and humans, we motivate future genetic studies that could lead to the complete identification of the mechanisms of TRM maintenance in humans.
Subjects/Keywords: Immunology; T cells; Genetic transcription
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Cvetkovski, F. (2019). Transcriptional control of tissue-resident memory T cell generation. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/d8-n16c-b343
Chicago Manual of Style (16th Edition):
Cvetkovski, Filip. “Transcriptional control of tissue-resident memory T cell generation.” 2019. Doctoral Dissertation, Columbia University. Accessed March 04, 2021.
https://doi.org/10.7916/d8-n16c-b343.
MLA Handbook (7th Edition):
Cvetkovski, Filip. “Transcriptional control of tissue-resident memory T cell generation.” 2019. Web. 04 Mar 2021.
Vancouver:
Cvetkovski F. Transcriptional control of tissue-resident memory T cell generation. [Internet] [Doctoral dissertation]. Columbia University; 2019. [cited 2021 Mar 04].
Available from: https://doi.org/10.7916/d8-n16c-b343.
Council of Science Editors:
Cvetkovski F. Transcriptional control of tissue-resident memory T cell generation. [Doctoral Dissertation]. Columbia University; 2019. Available from: https://doi.org/10.7916/d8-n16c-b343

Columbia University
21.
Dang, Alex Phu-Cuong.
Electrospun antibody-functionalized poly(dimethyl siloxane)-based meshes for improved T cell expansion.
Degree: 2018, Columbia University
URL: https://doi.org/10.7916/D8KW6ZGD
► Adoptive cell transfer (ACT) has garnered significant interest in recent years within the medical field due to its potential in providing an effective form of…
(more)
▼ Adoptive cell transfer (ACT) has garnered significant interest in recent years within the medical field due to its potential in providing an effective form of personalized medicine for patients suffering from a wide range of chronic illnesses, including but not limited to cancer. By leveraging the patient’s own cells as the therapeutic agent, concerns over patient compatibility and adverse reactions are significantly reduced. Central to this therapy is the ability to optimize cell quantity and cell activation in order to produce a more robust infusion to the patient.
This thesis focuses on two main aspects. The first is the materials synthesis and development of a novel platform for the ex vivo expansion of human T cells for ACT, while the second aims to elucidate the underlying structural mechanics of this platform. This platform, which consists of an electrospun mesh of micron and sub-micron diameter poly (dimethyl siloxane)-based fibers, aims to maintain the high surface-area to volume ratio characteristic of the current clinical gold standard. This also simultaneously allows for effective leveraging of T cell mechanosensing, a phenomenon previously discovered by our lab that is the ability of a human T cell to respond differently to surface mechanical cues. By modulating the concentration of poly (ε-caprolactone) in these fibers, a biocompatible polymer, the mesh mechanical rigidity was varied: this effectively allowed for the leverage of T cell mechanosensing by maintaining a low and tunable Young’s modulus throughout. Additionally, safety concerns involving transfusion of the expansion platform into the patient were addressed by having a single continuous substrate instead of an array of disjoint ferromagnetic beads.
Our results thus far indicate that this soft mesh platform can produce upwards of 5.6-12.5 times more T cells in healthy patients than the clinical gold standard while maintaining comparable levels of cellular activation and phenotypic distributions as measured through IFNγ secretion and expression of surface proteins CD107b, CD45RO, and CCR7, respectively. Additionally, this platform demonstrates the ability to produce improved expansion of exhausted (PD-1high) T cells from CLL patients compared to the clinical gold standard across all analyzed Rai stages. Finally, experiments have shown our platform to be scalable to produce clinically relevant levels of cells (> 50 million) from a given starting population, thus indicating its potential in adaptation in larger scale in vitro systems. The currently demonstrated capabilities of our mesh platform thus hold significant promise in the clinical development and adoption of ACT, as well as the development of larger scale in vitro systems.
In order to elucidate the underlying structural mechanics of our platform, quantitative AFM studies have indicated a force-dependency in rigidity measurement, thus indicating that standard Hertzian contact models and their derivatives (DMT, Sneddon, etc.), may not be ideal in calculating the rigidity…
Subjects/Keywords: Biomedical engineering; Immunology; T cells
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Dang, A. P. (2018). Electrospun antibody-functionalized poly(dimethyl siloxane)-based meshes for improved T cell expansion. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/D8KW6ZGD
Chicago Manual of Style (16th Edition):
Dang, Alex Phu-Cuong. “Electrospun antibody-functionalized poly(dimethyl siloxane)-based meshes for improved T cell expansion.” 2018. Doctoral Dissertation, Columbia University. Accessed March 04, 2021.
https://doi.org/10.7916/D8KW6ZGD.
MLA Handbook (7th Edition):
Dang, Alex Phu-Cuong. “Electrospun antibody-functionalized poly(dimethyl siloxane)-based meshes for improved T cell expansion.” 2018. Web. 04 Mar 2021.
Vancouver:
Dang AP. Electrospun antibody-functionalized poly(dimethyl siloxane)-based meshes for improved T cell expansion. [Internet] [Doctoral dissertation]. Columbia University; 2018. [cited 2021 Mar 04].
Available from: https://doi.org/10.7916/D8KW6ZGD.
Council of Science Editors:
Dang AP. Electrospun antibody-functionalized poly(dimethyl siloxane)-based meshes for improved T cell expansion. [Doctoral Dissertation]. Columbia University; 2018. Available from: https://doi.org/10.7916/D8KW6ZGD

University of Oxford
22.
Huo, Jiandong.
System-level analysis of early signalling in T cells.
Degree: PhD, 2012, University of Oxford
URL: http://ora.ox.ac.uk/objects/uuid:dcff1741-bd39-4b5b-a11b-99277d55890d
;
http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588401
► The prevailing view of signal transduction is that it proceeds through the linear relay of information via sequential bimolecular interactions, involving, for example, Src homology…
(more)
▼ The prevailing view of signal transduction is that it proceeds through the linear relay of information via sequential bimolecular interactions, involving, for example, Src homology (SH) 2 domains. It has been assumed that such interactions are highly selective, i.e. that the affinities of these interactions are several orders of magnitude higher than that for non-specific interactions. However, recent studies have suggested that the difference in affinities between so-called specific and non-specific interactions is not sufficient to support such a proposal. This therefore raises the question of how signalling pathway specificity is generated at all. To address this, we have taken a systems approach by expressing and purifying >90% of the SH2 domains identified in a T cell line using a next-generation sequencing-based transcriptomic analysis, and performed a systematic survey of the interaction of these SH2 domains with a set of potential phosphorylated peptides derived from the key signalling receptors of the T cell (including CD28, CTLA-4, PD-1, ICOS, BTLA, LAT and the CD3 subunits of the TCR complex), using surface plasmon resonance-based binding assays. Our results show that, instead of being highly selective for certain SH2 domains, the T cell-expressed receptors are very cross-reactive, such that each receptor is found to interact with ~50 different SH2 domains on average. In silico analysis based on these results confirms the expectation that affinity itself is not the sole determining factor for receptor specificity. Further exploration of the system using in silico simulations incorporating the absolute concentrations of SH2 domain-containing proteins measured in T cells using a proteomics-based approach, suggests instead that the specificity of SH2 domain recruitment by T-cell receptors is the result of systems effects, with expression levels of the signalling proteins being a major factor. Surprisingly, LCK, the most highly expressed SH2 domain in resting Jurkat, is predicted to dominate the binding of most receptors, suggesting a novel mechanism of Src kinase activation and function.
Subjects/Keywords: 571.966; Immunology; signalling; T cells
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APA (6th Edition):
Huo, J. (2012). System-level analysis of early signalling in T cells. (Doctoral Dissertation). University of Oxford. Retrieved from http://ora.ox.ac.uk/objects/uuid:dcff1741-bd39-4b5b-a11b-99277d55890d ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588401
Chicago Manual of Style (16th Edition):
Huo, Jiandong. “System-level analysis of early signalling in T cells.” 2012. Doctoral Dissertation, University of Oxford. Accessed March 04, 2021.
http://ora.ox.ac.uk/objects/uuid:dcff1741-bd39-4b5b-a11b-99277d55890d ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588401.
MLA Handbook (7th Edition):
Huo, Jiandong. “System-level analysis of early signalling in T cells.” 2012. Web. 04 Mar 2021.
Vancouver:
Huo J. System-level analysis of early signalling in T cells. [Internet] [Doctoral dissertation]. University of Oxford; 2012. [cited 2021 Mar 04].
Available from: http://ora.ox.ac.uk/objects/uuid:dcff1741-bd39-4b5b-a11b-99277d55890d ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588401.
Council of Science Editors:
Huo J. System-level analysis of early signalling in T cells. [Doctoral Dissertation]. University of Oxford; 2012. Available from: http://ora.ox.ac.uk/objects/uuid:dcff1741-bd39-4b5b-a11b-99277d55890d ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588401
23.
Prodger, Jessica L.
Defining Immune Correlates of HIV Susceptibility in the Foreskin.
Degree: 2014, University of Toronto
URL: http://hdl.handle.net/1807/65727
► HIV is a predominantly sexually transmitted infection that has infected over 60 million people and been responsible for 60 million deaths. To date, non-antiretroviral microbicides…
(more)
▼ HIV is a predominantly sexually transmitted infection that has infected over 60 million people and been responsible for 60 million deaths. To date, non-antiretroviral microbicides have failed to prevent HIV acquisition, or even increased it. This is likely because HIV preferentially infects activated immune cells (CD4+ T cells), taking advantage of the body’s attempts to defend itself. Therefore, relative immunoquiescence, as opposed to immune activation, may be protective. I hypothesized that men who are biologically more susceptible to HIV would have increased foreskin CD4 T cell activation, while the opposite would be true of men who are relatively resistant. The foreskin has recently been identified as a major site of HIV acquisition, but little previous research has been performed on this tissue. I therefore developed novel techniques to isolate viable, immunologically functional T cells from foreskin tissue. I then worked with the Rakai Health Sciences Program in Uganda to identify men undergoing elective circumcision who are HIV-Exposed but have remained SeroNegative (HESN, relatively resistant to HIV), and men with Herpes Simple Virus-2 infection (HSV-2+, relatively susceptible to HIV). I collected sub-preputial swabs and foreskin tissue from these men, and characterized numerous immune parameters in their samples. I found that HSV-2+ men had an increased relative abundance of CD4 T cells co-expressing the HIV receptor CCR5. In contrast, I found that HESN men had a decreased relative abundance of activated T cells (CD4/8 T cells producing TNFα) and Th17 cells (a pro-inflammatory T cell subset known to be particularly susceptible to HIV). Additionally, foreskin secretions from HESN men were more likely to have antibodies (IgA) able to neutralize HIV, and had more innate anti-viral peptides. I therefore propose HIV resistance may be driven by decreased T cell activation in genital tissue, in combination with increased secretion of anti-HIV immune proteins.
PhD
Advisors/Committee Members: Kaul, Rupert, Medical Science.
Subjects/Keywords: HIV; T cells; Circumcision; 0379
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MLA ·
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APA (6th Edition):
Prodger, J. L. (2014). Defining Immune Correlates of HIV Susceptibility in the Foreskin. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/65727
Chicago Manual of Style (16th Edition):
Prodger, Jessica L. “Defining Immune Correlates of HIV Susceptibility in the Foreskin.” 2014. Doctoral Dissertation, University of Toronto. Accessed March 04, 2021.
http://hdl.handle.net/1807/65727.
MLA Handbook (7th Edition):
Prodger, Jessica L. “Defining Immune Correlates of HIV Susceptibility in the Foreskin.” 2014. Web. 04 Mar 2021.
Vancouver:
Prodger JL. Defining Immune Correlates of HIV Susceptibility in the Foreskin. [Internet] [Doctoral dissertation]. University of Toronto; 2014. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/1807/65727.
Council of Science Editors:
Prodger JL. Defining Immune Correlates of HIV Susceptibility in the Foreskin. [Doctoral Dissertation]. University of Toronto; 2014. Available from: http://hdl.handle.net/1807/65727

University of Melbourne
24.
Lin, Wen Xu.
Study of regulatory T cells in transplantation.
Degree: 2011, University of Melbourne
URL: http://hdl.handle.net/11343/36958
► Transplantation has prolonged the survival of patients with terminal organ diseases. However, even with today’s advanced immunosuppressive therapies, graft rejection remains a major concern with…
(more)
▼ Transplantation has prolonged the survival of patients with terminal organ diseases. However, even with today’s advanced immunosuppressive therapies, graft rejection remains a major concern with significant patient morbidity and mortality still being associated with immunosuppressive medications. Tolerance induction has been a goal in transplantation for many years, although it still remains elusive. Recently, interest has been renewed in a subset of T cells, the regulatory T cells (Treg) and their potential role in tolerance induction. These cells demonstrate immunosuppressive potential in experimental models. This thesis focuses on examining the role of Treg in transplantation.
Techniques to characterise and genetically engineer Treg in vitro were developed. Our studies in over 200 transplant recipients (renal and liver) have shown: (1) percentages of CD4+CD25+ (“activated”) cells and CD4+CD25+Foxp3+ cells are significantly lower in RTR compared to controls; (2) percentages of “activated” cells are significantly lower in LTR compared to controls, while the percentages of CD4+CD25+Foxp3+ cells are significantly higher in patients with chronic liver diseases and LTR compared to normal controls; (3) the key finding that the proportion of “activated” cells expressing Foxp3+ cells is higher in RTR and correlates with renal allograft function; (4) the proportion of CD4+CD25+Foxp3+ cells do not alter at different times post-transplant; (5) a higher percentage of CD4+CD25+ cells is observed in recipients with malignancy; (6) incorporation of human Foxp3 in a human T cell line, CEM may induce a Treg-like phenotype. Collectively, the results from this project provide significant insight into the role of Treg in clinical transplantation and the role of the important Treg transcriptional regulator, Foxp3, in Treg induction and developing therapeutic strategies to facilitate graft acceptance by extending the use of Treg in the future. These findings may help to add further information regarding the mechanism of tolerance induction that may lead to graft survival without ongoing drug therapy.
Subjects/Keywords: regulatory T cells; transplantation
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Lin, W. X. (2011). Study of regulatory T cells in transplantation. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/36958
Chicago Manual of Style (16th Edition):
Lin, Wen Xu. “Study of regulatory T cells in transplantation.” 2011. Doctoral Dissertation, University of Melbourne. Accessed March 04, 2021.
http://hdl.handle.net/11343/36958.
MLA Handbook (7th Edition):
Lin, Wen Xu. “Study of regulatory T cells in transplantation.” 2011. Web. 04 Mar 2021.
Vancouver:
Lin WX. Study of regulatory T cells in transplantation. [Internet] [Doctoral dissertation]. University of Melbourne; 2011. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/11343/36958.
Council of Science Editors:
Lin WX. Study of regulatory T cells in transplantation. [Doctoral Dissertation]. University of Melbourne; 2011. Available from: http://hdl.handle.net/11343/36958

University of Melbourne
25.
Ross, Ellen Margaret.
Autoantigen-specific regulatory T cells in autoimmunity.
Degree: 2012, University of Melbourne
URL: http://hdl.handle.net/11343/38044
► In order to protect the host from disease, the immune system is equipped with the capacity to recognise and respond to a plethora of pathogens.…
(more)
▼ In order to protect the host from disease, the immune system is equipped with the capacity to recognise and respond to a plethora of pathogens. Given the breadth of the specificities that the immune system will react to, it is remarkable that the tissues and organs that constitute self avoid immune-mediated damage. Injury to self does not occur because the immune systemic is educated, through a variety of mechanisms, to distinguish between antigens that constitute self and those antigens that are foreign, a collective process which is termed immune tolerance. Immune tolerance is an extremely important process, as made most evident by the development of immune-mediated damage and autoimmune disease that occurs when immune tolerance is not upheld, the outcomes of which can be potentially catastrophic. Understanding the intricacies of immune tolerance will be beneficial in discerning why some individuals develop autoimmune disease, and will also aid in the identification of strategies which can potentially be utilised for the treatment of autoimmune disease.
Experimental autoimmune gastritis in mice is an excellent model of human autoimmune gastritis and is therefore a useful tool for the study of autoimmune disease and tolerance. Experimental autoimmune gastritis is a very well characterised disease, as the molecular, cellular and genetic aspects of the disease have been well studied. The disease is characterised by a CD4+ T cell mediated immune response that is directed towards the α and β subunits of the gastric H+/K+-ATPase, which is the autoantigen target in both murine and human autoimmune gastritis. Within the thymus, expression of the H/Kβ is, at best, barely detectable, and this compromises the presentation of H/Kα, which is unstable and therefore rapidly degraded in the absence of H/Kβ. As a result, thymic events appear to contribute little in the maintenance of tolerance to the H+/K+-ATPase, and for this reason it is likely that tolerogenic events in the periphery will be paramount. An important component of peripheral tolerance is the regulatory T cell population, as these cells are required throughout life to maintain peripheral immune homeostasis in order to avoid the development of autoimmunity. Regulatory T cells may well be important in maintaining peripheral tolerance to the H+/K+-ATPase given the lack of thymic tolerogenic events that occur in response to this autoantigen. The aim of this investigation was to investigate the role of regulatory T cells in maintaining tolerance to the H+/K+-ATPase.
The work presented in Chapter 3 reaffirms that H/Kα-specific regulatory T cells do not develop with the thymus, but instead can be generated de novo in the periphery following contact with the H/Kα. Induced H/Kα-specific regulatory T cells are shown to be suppressive and following this, an investigation into the mechanisms that drive the extrathymic generation of H/Kα-specific regulatory T cells indicated that…
Subjects/Keywords: regulatory T cells; autoimmunity; tolerance
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Ross, E. M. (2012). Autoantigen-specific regulatory T cells in autoimmunity. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/38044
Chicago Manual of Style (16th Edition):
Ross, Ellen Margaret. “Autoantigen-specific regulatory T cells in autoimmunity.” 2012. Doctoral Dissertation, University of Melbourne. Accessed March 04, 2021.
http://hdl.handle.net/11343/38044.
MLA Handbook (7th Edition):
Ross, Ellen Margaret. “Autoantigen-specific regulatory T cells in autoimmunity.” 2012. Web. 04 Mar 2021.
Vancouver:
Ross EM. Autoantigen-specific regulatory T cells in autoimmunity. [Internet] [Doctoral dissertation]. University of Melbourne; 2012. [cited 2021 Mar 04].
Available from: http://hdl.handle.net/11343/38044.
Council of Science Editors:
Ross EM. Autoantigen-specific regulatory T cells in autoimmunity. [Doctoral Dissertation]. University of Melbourne; 2012. Available from: http://hdl.handle.net/11343/38044

University of Cambridge
26.
Strege, Katharina.
Identifying regulators of cytotoxic T cell function through molecular and genetic screening.
Degree: PhD, 2019, University of Cambridge
URL: https://doi.org/10.17863/CAM.40639
;
https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782806
► Cytotoxic T lymphocytes (CTL) are crucial components of the adaptive immune system that kill infected and tumourigenic cells. CTL killing requires focused secretion of cytotoxic…
(more)
▼ Cytotoxic T lymphocytes (CTL) are crucial components of the adaptive immune system that kill infected and tumourigenic cells. CTL killing requires focused secretion of cytotoxic compounds from lytic granules. This process is known as degranulation. In this study, I aimed to establish the CRISPR-Cas9 gene editing technology in primary T cells and to optimise screening approaches to identify regulators of CTL killing. The first half of the thesis focuses on primary mouse CTL. The CRISPR technology was successfully optimised in CTL using Cas9-ribonucleoprotein complexes resulting in efficient CRISPR-mediated loss of target proteins. Genes encoding known mediators of CTL cytotoxicity, Rab27a Munc13-4 and Prf1, were targeted using CRISPR. The resulting samples were used to establish a flow cytometry-based assay that simultaneously measures CTL degranulation and target cell death. This assay enabled me to screen for mediators of CTL killing, while providing mechanistic insight by detecting degranulation. The screen was informed by a transcriptomic study that compared naive and effector CD8 T cells. 1803 significantly upregulated differentially expressed genes [log2(fold change) > 2] were identified. Functional annotation analysis and literature research were used to select genes for the targeted CRISPR screen, which highlighted the importance of HIF-1α and NFIL3 in CTL killing. The second half of the thesis focuses on primary human CTL. The combined degranulation and killing assay was further validated using patient-derived CTL, indicating its potential as a diagnostic test. I showed that the assay is suitable for mid-sized screens using a library of 64 compounds targeting the NF-κB signalling pathway. Further opportunities for increasing the scale of this screening technique are discussed. Finally, I successfully tested CRISPR using Cas9-ribonucleoprotein complexes in the human system. Additionally, stable Cas9 expression through lentiviral transduction was explored in primary CTL and related cell lines. This has the potential to allow selection of cells expressing the CRISPR machinery, providing a cleaner experimental system and the possibility of large-scale screening approaches. In summary, the techniques established in this thesis will be valuable for studying the genetics underlying CTL killing and the combined degranulation and killing assay furthermore shows great potential for diagnostic purposes.
Subjects/Keywords: Cytotoxic T cells; CRISPR; screening
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Strege, K. (2019). Identifying regulators of cytotoxic T cell function through molecular and genetic screening. (Doctoral Dissertation). University of Cambridge. Retrieved from https://doi.org/10.17863/CAM.40639 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782806
Chicago Manual of Style (16th Edition):
Strege, Katharina. “Identifying regulators of cytotoxic T cell function through molecular and genetic screening.” 2019. Doctoral Dissertation, University of Cambridge. Accessed March 04, 2021.
https://doi.org/10.17863/CAM.40639 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782806.
MLA Handbook (7th Edition):
Strege, Katharina. “Identifying regulators of cytotoxic T cell function through molecular and genetic screening.” 2019. Web. 04 Mar 2021.
Vancouver:
Strege K. Identifying regulators of cytotoxic T cell function through molecular and genetic screening. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Mar 04].
Available from: https://doi.org/10.17863/CAM.40639 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782806.
Council of Science Editors:
Strege K. Identifying regulators of cytotoxic T cell function through molecular and genetic screening. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://doi.org/10.17863/CAM.40639 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782806

University of Cambridge
27.
Alam, Rafeah.
T cell phenotyping of a mouse model of Activated PI3Kdelta Syndrome.
Degree: PhD, 2019, University of Cambridge
URL: https://doi.org/10.17863/CAM.40724
;
https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782758
► Activated PI3Kdelta Syndrome (APDS) is immunodeficiency caused by a heterozygous gain-of-function mutation (E1021K) in the PIK3CD gene, encoding for the p110delta catalytic subunit of phosphoinositide…
(more)
▼ Activated PI3Kdelta Syndrome (APDS) is immunodeficiency caused by a heterozygous gain-of-function mutation (E1021K) in the PIK3CD gene, encoding for the p110delta catalytic subunit of phosphoinositide 3-kinase (PI3K). APDS patients are lymphopenic, suffer from sinopulmonary infections and from increased susceptibility to bacterial and herpes group virus infections. Following T cell receptor (TCR) stimulation, T cells from these patients undergo increased activation induced cell death, which can be reversed by selective PI3Kdelta inhibitors. I used a new conditional knock-in mouse (T-p110delta E1020K) in order to investigate the effect of hyperactive p110delta on T cell function. Hyperactivation of p110delta led to increased PIP3 and pAKT levels following TCR stimulation that was reduced using a selective p110delta inhibitor. Following in vitro TCR stimulation, T cells proliferated normally but showed increased apoptosis that was reversed by a p110delta specific inhibitor. Despite enhanced apoptosis, CD8+ T cells displayed enhanced activation that was associated with increased levels of cytokines and granzyme B. CD4+ T cells with hyperactive p110delta produced increased Th1, Th2, Th17 and Tfh cytokines but showed reduced Treg differentiation in vitro. Conditional T-p110delta E1020K mice have reduced Tregs in the thymus but increased peripheral Tregs. These mice also have increased numbers of T follicular helper cells and germinal centre (GC) B cells upon immunisation with a T cell dependent antigen (NP-KLH). Reduced antigen specific IgG1+ cells within GC B cells was detected in mice harbouring hyperactive p110delta mutation in B cells, implying that the antibody deficiencies observed in APDS patients is due to an intrinsic defect within B cells rather than limited help from T cells. T-p110delta E1020K mice mounted normal primary responses to acute infections .However adoptive transfer of ovalbumin-specific T cell receptor transgenic CD8 T cells (OT1) revealed an intrinsic defect in the primary expansion of CD8+ T cells with hyperactive p110delta. This defect in primary expansion was found to be rescued in the presence of wild type OT1 cells. Following infection with acute pathogens, CD8+ T cells with hyperactive p110delta displayed normal to increased effector function with phenotypically reduced memory cells as indicated by reduced memory precursor effectors cells (MPECs). In contrast, following chronic infection, T-p110delta E1020K displayed increased signs of T cell exhaustion that is also characteristic of APDS patients as they suffer from chronic herpes virus infections. This set of work therefore shows that the mouse model recapitulates key aspects of APDS patients and give insights into the role of p110delta signaling in different T cell subsets influenced by hyperactive p110delta activity. Further, in depth analysis of proteomics and gene array data of in vitro stimulated T cells generated during this study, can provide a better understanding of the mechanisms behind the T cell phenotype observed.
Subjects/Keywords: APDS; PI3K; T cells
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Alam, R. (2019). T cell phenotyping of a mouse model of Activated PI3Kdelta Syndrome. (Doctoral Dissertation). University of Cambridge. Retrieved from https://doi.org/10.17863/CAM.40724 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782758
Chicago Manual of Style (16th Edition):
Alam, Rafeah. “T cell phenotyping of a mouse model of Activated PI3Kdelta Syndrome.” 2019. Doctoral Dissertation, University of Cambridge. Accessed March 04, 2021.
https://doi.org/10.17863/CAM.40724 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782758.
MLA Handbook (7th Edition):
Alam, Rafeah. “T cell phenotyping of a mouse model of Activated PI3Kdelta Syndrome.” 2019. Web. 04 Mar 2021.
Vancouver:
Alam R. T cell phenotyping of a mouse model of Activated PI3Kdelta Syndrome. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Mar 04].
Available from: https://doi.org/10.17863/CAM.40724 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782758.
Council of Science Editors:
Alam R. T cell phenotyping of a mouse model of Activated PI3Kdelta Syndrome. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://doi.org/10.17863/CAM.40724 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782758

University of Montana
28.
Osborne, Douglas Grant.
Biological effects of trogocytosis on CD4+ T lymphocytes.
Degree: PhD, 2013, University of Montana
URL: https://scholarworks.umt.edu/etd/100
► Antigen recognition by CD4+ T cells leads to large-scale spatial and temporal molecular redistributions, forming the immunological synapse. We have previously shown that upon…
(more)
▼ Antigen recognition by CD4+ T cells leads to large-scale spatial and temporal molecular redistributions, forming the immunological synapse. We have previously shown that upon dissociation, T cells capture large membrane fragments from antigen-presenting cells directly from the immunological synapse. The mechanism and biological significance of this process, termed trogocytosis, is still unclear. In this thesis I examined the impact that trogocytosis has on the individual T cell after capturing molecules from the antigen presenting cell. I employed murine fibroblast cell lines expressing an I-Ek molecule loaded with a covalently attached antigenic peptide (moth cytochrome C 88-103) and with or without a GFP-tagged cytoplasmic tail as antigen presenting cells for T cells from a peptide-specific TCR transgenic mouse. Using a combination of high-resolution microscopy and flow cytometry, In this thesis I showed that the trogocytosed material is retained on the surface of the T cell and is associated with sustained signaling after removal of the antigen presenting cells. The intercellular trogocytosis correlates with alterations in and is associated with sustained survival of the trogocytosis-positive (trog+) cells in vitro. I also showed that sustained signaling in trog+ T cells occurs at the trogocytosed spot and is initiated by the trogocytosed material. I conclude, that after trogocytosis, trog+ T cells present antigen and induce activation of antigen-specific naïve T cells. The findings from this thesis will help to elucidate the role of trogocytosis on CD4+ T cells.
Subjects/Keywords: T cells; trogocytosis; CD4; imaging
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APA ·
Chicago ·
MLA ·
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Export
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APA (6th Edition):
Osborne, D. G. (2013). Biological effects of trogocytosis on CD4+ T lymphocytes. (Doctoral Dissertation). University of Montana. Retrieved from https://scholarworks.umt.edu/etd/100
Chicago Manual of Style (16th Edition):
Osborne, Douglas Grant. “Biological effects of trogocytosis on CD4+ T lymphocytes.” 2013. Doctoral Dissertation, University of Montana. Accessed March 04, 2021.
https://scholarworks.umt.edu/etd/100.
MLA Handbook (7th Edition):
Osborne, Douglas Grant. “Biological effects of trogocytosis on CD4+ T lymphocytes.” 2013. Web. 04 Mar 2021.
Vancouver:
Osborne DG. Biological effects of trogocytosis on CD4+ T lymphocytes. [Internet] [Doctoral dissertation]. University of Montana; 2013. [cited 2021 Mar 04].
Available from: https://scholarworks.umt.edu/etd/100.
Council of Science Editors:
Osborne DG. Biological effects of trogocytosis on CD4+ T lymphocytes. [Doctoral Dissertation]. University of Montana; 2013. Available from: https://scholarworks.umt.edu/etd/100

University of New South Wales
29.
Pollock, Abigail Hazel.
How dietary lipids and membrane order affect T cell function in vivo.
Degree: Centre for Vascular Research, 2013, University of New South Wales
URL: http://handle.unsw.edu.au/1959.4/53561
;
https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12258/SOURCE02?view=true
► As the T cell receptor and many of the associated signalling molecules are embedded within the plasma membrane, it has been hypothesised that plasma membrane…
(more)
▼ As the
T cell receptor and many of the associated signalling molecules are embedded within the plasma membrane, it has been hypothesised that plasma membrane lipids, and associated lipid ‘ordered’ membrane domains, play a role in regulating
T cell signalling. The first aim of this thesis was to examine in mice whether dietary lipids influence the lipid composition of
T cells and thus membrane order, and how this correlates to in vivo and ex vivo
T cell responses. Chapters 3 and 4 describe both acute and long-term dietary studies, which involved feeding C57BL/6J and LDLR-/- mice a high-fat or high-cholesterol diet. A contact hypersensitivity (CHS) reaction was then induced using 1-fluoro-2,4-dinitrobenzene and the CD4+ and CD8+
T cell responses examined in the draining lymph nodes by flow cytometry. The in vivo
T cell responses were correlated to the cellular lipid content of splenic
T cells using mass spectrometry, and membrane order measured with Laurdan microscopy. Finally, the activation response of ex vivo stimulated splenic
T cells was assessed with qRT-PCR. Both the C57BL/6J and LDLR-/- dietary studies illustrated that long-term high-fat or high-cholesterol feeding significantly increased both CD4+ and CD8+
T cell proliferation, and central-memory CD4+
T cell production, within the draining lymph nodes following CHS. This was associated with changes in cellular phospholipids, fatty acids and cholesterol, as well as alterations in membrane order at the
T cell activation site, and reduced IL-2 mRNA production. The last results chapter of this thesis, chapter 5, focused directly on how membrane order impacts on
T cell function in vivo. Using an adoptive transfer system, CD4+
T cells from OT-II transgenic mice were treated with the oxysterol 7-ketocholesterol, which perturbs membrane condensation, or a cholesterol control, before transfer into B6.SJL recipient mice. I then challenged the recipients with ovalbumin323–339 to measure antigen-specific CD4+
T cell responses by flow cytometry, which were again correlated the sterol content of ex vivo manipulated
cells. Our results were inconsistent but suggest that both 7KC and cholesterol treatment cause a reduction in OVA-specific CD4+
T cell proliferation within the draining lymph nodes of recipient mice.
Advisors/Committee Members: Gaus, Katharina, Centre for Vascular Research, Faculty of Medicine, UNSW, Tedla, Nicodemus, Faculty of Medicine, UNSW.
Subjects/Keywords: Lipids; T cells; Membrane order
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APA (6th Edition):
Pollock, A. H. (2013). How dietary lipids and membrane order affect T cell function in vivo. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/53561 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12258/SOURCE02?view=true
Chicago Manual of Style (16th Edition):
Pollock, Abigail Hazel. “How dietary lipids and membrane order affect T cell function in vivo.” 2013. Doctoral Dissertation, University of New South Wales. Accessed March 04, 2021.
http://handle.unsw.edu.au/1959.4/53561 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12258/SOURCE02?view=true.
MLA Handbook (7th Edition):
Pollock, Abigail Hazel. “How dietary lipids and membrane order affect T cell function in vivo.” 2013. Web. 04 Mar 2021.
Vancouver:
Pollock AH. How dietary lipids and membrane order affect T cell function in vivo. [Internet] [Doctoral dissertation]. University of New South Wales; 2013. [cited 2021 Mar 04].
Available from: http://handle.unsw.edu.au/1959.4/53561 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12258/SOURCE02?view=true.
Council of Science Editors:
Pollock AH. How dietary lipids and membrane order affect T cell function in vivo. [Doctoral Dissertation]. University of New South Wales; 2013. Available from: http://handle.unsw.edu.au/1959.4/53561 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12258/SOURCE02?view=true

University of Aberdeen
30.
Pappalardo, Angela.
Defining the role of γδ cells in bone loss associated with chronic inflammation.
Degree: PhD, 2013, University of Aberdeen
URL: https://abdn.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152657240005941
;
https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589513
► The extensive infiltration of immune cells in the joints of patients affected by rheumatoid arthritis (RA), and the subsequent production of pro-inflammatory cytokines triggers bone…
(more)
▼ The extensive infiltration of immune cells in the joints of patients affected by rheumatoid arthritis (RA), and the subsequent production of pro-inflammatory cytokines triggers bone erosion through the extensive stimulation of bone resorbing osteoclasts (OCs). The activity of γδ T cells has been implicated to influence the onset and severity of the disease pathology in murine models of human RA. With this study the effects of γδ T cells for influencing OC differentiation and resorptive activity were assessed in vitro. Activated γδ T cells exerted inhibitory effects on OC differentiation and resorptive activity, these effects were mediated by the release of soluble factors, since similar inhibitory effects were obtained using conditioned medium (CM) from activated γδ T cells. The primary mediator of such effects was determined to be IFN, since neutralisation markedly restored OC differentiation and resorptive activity. γδ T cell proliferation, activation and survival following culture with autologous mature OCs were assessed by flow cytometry. Interestingly, OCs and OC-derived CM induced activation of γδ T cells as determined by the expression of the early activation marker CD69. A mediator of this stimulatory effect on T cells was found to be TNF, since neutralisation of TNFα decreased the stimulatory effect of OCs on CD69 expression. Consistently, OCs, but not OC-derived CM, increased the proliferation of IL-2-stimulated γδ T cells and also supported the survival of resting γδ T cells. This study provides new insights into the in vitro interactions between human γδ T cells and OCs, moreover it defines osteoclasts as immune competent cells capable of influencing the activation status and the viability of T lymphocytes, and provide evidence for a novel stimulatory effect of OCs on γδ T cells.
Subjects/Keywords: 616.7; Osteoclast inhibition; T cells
Record Details
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Record Details
Similar Records
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Pappalardo, A. (2013). Defining the role of γδ cells in bone loss associated with chronic inflammation. (Doctoral Dissertation). University of Aberdeen. Retrieved from https://abdn.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152657240005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589513
Chicago Manual of Style (16th Edition):
Pappalardo, Angela. “Defining the role of γδ cells in bone loss associated with chronic inflammation.” 2013. Doctoral Dissertation, University of Aberdeen. Accessed March 04, 2021.
https://abdn.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152657240005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589513.
MLA Handbook (7th Edition):
Pappalardo, Angela. “Defining the role of γδ cells in bone loss associated with chronic inflammation.” 2013. Web. 04 Mar 2021.
Vancouver:
Pappalardo A. Defining the role of γδ cells in bone loss associated with chronic inflammation. [Internet] [Doctoral dissertation]. University of Aberdeen; 2013. [cited 2021 Mar 04].
Available from: https://abdn.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152657240005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589513.
Council of Science Editors:
Pappalardo A. Defining the role of γδ cells in bone loss associated with chronic inflammation. [Doctoral Dissertation]. University of Aberdeen; 2013. Available from: https://abdn.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152657240005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589513
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