subject:(innate immunity)

Texas A&M University

1. Tan, Peng. DISSECTING THE ROLES OF WHIP-TRIM14-PPP6C IN INNATE ANTIVIRAL IMMUNITY AND MYELOID BECLIN1 IN TUMOR IMMUNITY.

Degree: PhD, Medical Sciences, 2018, Texas A&M University

URL: http://hdl.handle.net/1969.1/173576

► The innate immune system has the ability to tune the inflammatory environment by modulating pathogen-recognition receptors (PRRs) signaling, which can either induce oncogenic changes or… (more)

▼ The innate immune system has the ability to tune the inflammatory environment by modulating pathogen-recognition receptors (PRRs) signaling, which can either induce oncogenic changes or generate antitumor immunity through cross-talking with adaptive immunity. Thus, tight regulation of innate immune signaling pathways is essential either for an effective immune response against viral infections and tumor or for preventing detrimental autoimmunity. Mitochondrial antiviral-signaling protein MAVS acts as a central hub for RIG-I receptor proximal signal propagation. However, key components in the assembly of the MAVS mitochondrial platform that promote RIG-I mitochondrial localization and optimal activation are still largely undefined. Employing pooled RNAi and yeast two-hybrid screenings, we report that the mitochondrial adaptor protein TRIM14 provides a docking platform for the assembly of the mitochondrial signaling complex required for maximal activation of RIG-I-mediated signaling, consisting of WHIP and protein phosphatase PPP6C. Following viral infection, the ubiquitin-binding domain in WHIP bridges RIG-I with MAVS through the binding to polyUb chains of RIGI at lysine 164. ATPase domain in WHIP contributes to the stabilization of RIG-I-dsRNA interaction. Moreover, phosphatase PPP6C is responsible for RIG-I dephosphorylation. Together, our findings define the WHIP-TRIM14-PPP6C mitochondrial signalosome required for RIG-I-mediated innate antiviral immunity. Giving the embryonic lethality of Beclin1 (Becn1) homozygous mice, roles of myeloid Becn1 in cancer-associated inflammation and tumor immunity remain elusive. We demonstrate herein that mice with myeloid loss of Becn1 (Becn1^ΔM) show high risk of precursor (pre)-B cell lymphoma associated with neutrophilia. Becn1 deficiency stabilizes neutrophil MEKK3 independent of autophagy, resulting in the aberrant p38 activation and exaggerated tumorigenic inflammation that triggers the expressions of PD-L1 and pro-survival genes in pre-B cells. Importantly, we identify low Becn1 expression of neutrophils correlates with programmed death ligand 1 (PD-L1) levels and cancer recurrence in patients with pre-B acute lymphoblastic lymphoma (ALL). In a mouse model of melanoma, expansion and infiltration of neutrophils and B cells due to Becn1 deficiency favor metastasis of B16 melanoma. Thus, homeostatic maintenance of Becn1 level in neutrophils will contribute to the outcome of the tumorigenic process of pre-B cells. Advisors/Committee Members: Moczygemba, Margie (advisor), Wang, Rongfu (advisor), Zhou, Yubin (committee member), Cao, Qi (committee member), Xu, Yi (committee member).

Subjects/Keywords: Innate Immunity; Tumor Immunity

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Tan, P. (2018). DISSECTING THE ROLES OF WHIP-TRIM14-PPP6C IN INNATE ANTIVIRAL IMMUNITY AND MYELOID BECLIN1 IN TUMOR IMMUNITY. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/173576

Chicago Manual of Style (16^th Edition):

Tan, Peng. “DISSECTING THE ROLES OF WHIP-TRIM14-PPP6C IN INNATE ANTIVIRAL IMMUNITY AND MYELOID BECLIN1 IN TUMOR IMMUNITY.” 2018. Doctoral Dissertation, Texas A&M University. Accessed January 23, 2021. http://hdl.handle.net/1969.1/173576.

MLA Handbook (7^th Edition):

Tan, Peng. “DISSECTING THE ROLES OF WHIP-TRIM14-PPP6C IN INNATE ANTIVIRAL IMMUNITY AND MYELOID BECLIN1 IN TUMOR IMMUNITY.” 2018. Web. 23 Jan 2021.

Vancouver:

Tan P. DISSECTING THE ROLES OF WHIP-TRIM14-PPP6C IN INNATE ANTIVIRAL IMMUNITY AND MYELOID BECLIN1 IN TUMOR IMMUNITY. [Internet] [Doctoral dissertation]. Texas A&M University; 2018. [cited 2021 Jan 23]. Available from: http://hdl.handle.net/1969.1/173576.

Council of Science Editors:

Tan P. DISSECTING THE ROLES OF WHIP-TRIM14-PPP6C IN INNATE ANTIVIRAL IMMUNITY AND MYELOID BECLIN1 IN TUMOR IMMUNITY. [Doctoral Dissertation]. Texas A&M University; 2018. Available from: http://hdl.handle.net/1969.1/173576

University of Alberta

2. Guntermann, Silvia. Caspase activity and regulation in Drosophila melanogaster innate immunity.

Degree: PhD, Department of Medical Microbiology and Immunology, 2014, University of Alberta

URL: https://era.library.ualberta.ca/files/cr207tp490

► The fine balance struck between life and death is key for the health of all multicellular organisms and therefore the pathways that govern life and… (more)

▼ The fine balance struck between life and death is key for the health of all multicellular organisms and therefore the pathways that govern life and death decisions are evolutionarily highly conserved. For example, the human TNF and the Drosophila IMD pathways coordinate signaling elements such as conserved JNK, NF-κB, and caspase modules to drive appropriate responses. Caspases are an evolutionarily conserved family of cysteinyl aspartate proteases with fundamental roles in the opposing processes of cell-survival and cell-death. The caspase Dredd is an essential pro-survival regulator of the IMD mediated immune response. However, the detailed involvement of Dredd in the sequential activation of the IMD cascade, the position of Dredd, and Dredd’s interactions with the IMD pathway were unknown. In addition, the molecular mechanism of Dredd activation and regulation was unclear. In this study I conducted a thorough structural and functional analysis of the mechanism of Dredd activity in IMD signaling. I revealed numerous interactions of Dredd with early activators of the IMD pathway. I showed that the caspase activity inhibitor p35 blocked Dredd activation in a mechanism that is distinct from the general mechanism of p35- dependent caspase inhibition. In addition, Dredd activation appears independent of auto-processing which might be explained by the lack of Dredd linker residues that support auto-processing and may explain Dredd’s sole function in pro- survival responses. In a combination of cell culture and in vivo assays, I demonstrated that Dredd is required for the activation of dJNK signaling upstream of dTAK1 and determined that Dredd additionally functions down- stream of Imd activation. Furthermore, my data uncovered a dual regulation of dIAP2 by RING domain mediated destruction and Dronc mediated N-terminal proteolytic cleavage. In summary, the data indicate a distinct activation mechanism for Dredd and establish dual functions for Dredd in the IMD signaling cascade, where Dredd is required in a proximal signaling complex for the early transduction of a phospho-relay to Rel and dJNK as well as for the subsequent activation of Rel. The data also uncover a novel role for Dronc in immune signaling. Combined the findings underline the importance and complexity of non-apoptotic roles of caspases.

Subjects/Keywords: innate immunity; caspase

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Guntermann, S. (2014). Caspase activity and regulation in Drosophila melanogaster innate immunity. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/cr207tp490

Chicago Manual of Style (16^th Edition):

Guntermann, Silvia. “Caspase activity and regulation in Drosophila melanogaster innate immunity.” 2014. Doctoral Dissertation, University of Alberta. Accessed January 23, 2021. https://era.library.ualberta.ca/files/cr207tp490.

MLA Handbook (7^th Edition):

Guntermann, Silvia. “Caspase activity and regulation in Drosophila melanogaster innate immunity.” 2014. Web. 23 Jan 2021.

Vancouver:

Guntermann S. Caspase activity and regulation in Drosophila melanogaster innate immunity. [Internet] [Doctoral dissertation]. University of Alberta; 2014. [cited 2021 Jan 23]. Available from: https://era.library.ualberta.ca/files/cr207tp490.

Council of Science Editors:

Guntermann S. Caspase activity and regulation in Drosophila melanogaster innate immunity. [Doctoral Dissertation]. University of Alberta; 2014. Available from: https://era.library.ualberta.ca/files/cr207tp490

Universiteit Utrecht

3. Hogenkamp, A. Collectins in innate immune defense of pigs and chickens.

Degree: 2007, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/23210

► In the Netherlands, the number of chickens and pigs exceeds the number of human inhabitants by far. Therefore, combating infections in livestock is not only… (more)

▼ In the Netherlands, the number of chickens and pigs exceeds the number of human inhabitants by far. Therefore, combating infections in livestock is not only of economical importance, but also of great importance to public health. The innate immune system provides a first line defense against infectious pathogens, and its effector mechanisms rely on the recognition of features that are common to many pathogens. These features, known as pathogen-associated molecular patterns can be recognized by pattern recognition molecules at the site of infection, which is often an epithelial surface like the lung, skin or gastro-intestinal tract. Collectins, an important group of pattern recognition molecules, have been reported to be expressed in many epithelial surfaces. In the lung, Surfactant Protein-D (SP-D) contributes to the maintenance of a sterile respiratory system. Its role in the gastro-intestinal tract, which is dominated by the presence of micro-organisms, is less clear. Therefore, we investigated the interaction of porcine SP-D (pSP-D) with various Gram-negative bacteria isolated from the porcine intestine. It was shown that while pSP-D is capable of reducing growth rates of E. coli K12, the growth rates and survival of pathogenic bacterial strains isolated from the porcine intestine remained unaffected. Furthermore, pSP-D was shown to affect bacterial adhesion- and invasion- characteristics, leading to a significant increase in adhesion and invasion of bacteria into IPI-I2 cells. It is not yet clear what the mechanism behind these effects is, but it could reflect a scavenger function for pSP-D in the intestine. In the chicken, only two collectins had been described thus far. In this thesis, we report the discovery of three new chicken collectins, chicken Collectin 1-3 (cCL-1, -2,and -3) and one chicken lectin, chicken Lung Lectin (cLL). Results from this study support the assumption that cCL-1, -2 and -3, together with their respective mammalian homologues CL-L1, CL-K1 and CL-P1 represent three new unique classes within the collectin protein family. Because of its predominant expression in the chicken respiratory tract, the newly discovered chicken lectin was designated chicken Lung Lectin (cLL). To investigate whether these chicken (col)lectins are involved in avian innate immunity, their mRNA expression levels during bacterial and viral infections were investigated. Samples derived from three infection-models were analyzed, and the results showed that mRNA expression of chicken (col)lectins cCL-1, cCL-2, cSP-A and cLL can be affected by both bacterial and viral infections. We also investigated the structural and functional aspects of cLL. To this end, recombinant cLL was successfully produced in HEK-293 EBNA cells. Characterization of recombinant cLL revealed that this protein is capable of binding sugars, and, as predicted from its sequence, does so in a calcium-dependent manner. In addition, cLL showed anti-viral activity against avian IAV in our preliminary tests, and HAA-inhibition of a human isolate of IAV…

Subjects/Keywords: Diergeneeskunde; collectin; innate immunity; chicken

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hogenkamp, A. (2007). Collectins in innate immune defense of pigs and chickens. (Doctoral Dissertation). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/23210

Chicago Manual of Style (16^th Edition):

Hogenkamp, A. “Collectins in innate immune defense of pigs and chickens.” 2007. Doctoral Dissertation, Universiteit Utrecht. Accessed January 23, 2021. http://dspace.library.uu.nl:8080/handle/1874/23210.

MLA Handbook (7^th Edition):

Hogenkamp, A. “Collectins in innate immune defense of pigs and chickens.” 2007. Web. 23 Jan 2021.

Vancouver:

Hogenkamp A. Collectins in innate immune defense of pigs and chickens. [Internet] [Doctoral dissertation]. Universiteit Utrecht; 2007. [cited 2021 Jan 23]. Available from: http://dspace.library.uu.nl:8080/handle/1874/23210.

Council of Science Editors:

Hogenkamp A. Collectins in innate immune defense of pigs and chickens. [Doctoral Dissertation]. Universiteit Utrecht; 2007. Available from: http://dspace.library.uu.nl:8080/handle/1874/23210

4. 舟見, 健児. Toll-like receptor 3の細胞内局在、及びシグナル伝達に関与する機能ドメインの同定 : The cytoplasmic "linker region" in Toll-like receptor 3 controls receptor licalization and signaling; Toll-like receptor 3 ノサイボウナイキョクザイオヨビシグナルデンタツニカンヨスルキノウドメインノドウテイ.

Degree: Nara Institute of Science and Technology / 奈良先端科学技術大学院大学

URL: http://hdl.handle.net/10061/2831

Subjects/Keywords: Innate immunity

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

舟見, �. (n.d.). Toll-like receptor 3の細胞内局在、及びシグナル伝達に関与する機能ドメインの同定 : The cytoplasmic "linker region" in Toll-like receptor 3 controls receptor licalization and signaling; Toll-like receptor 3 ノサイボウナイキョクザイオヨビシグナルデンタツニカンヨスルキノウドメインノドウテイ. (Thesis). Nara Institute of Science and Technology / 奈良先端科学技術大学院大学. Retrieved from http://hdl.handle.net/10061/2831

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

舟見, 健児. “Toll-like receptor 3の細胞内局在、及びシグナル伝達に関与する機能ドメインの同定 : The cytoplasmic "linker region" in Toll-like receptor 3 controls receptor licalization and signaling; Toll-like receptor 3 ノサイボウナイキョクザイオヨビシグナルデンタツニカンヨスルキノウドメインノドウテイ.” Thesis, Nara Institute of Science and Technology / 奈良先端科学技術大学院大学. Accessed January 23, 2021. http://hdl.handle.net/10061/2831.

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

舟見, 健児. “Toll-like receptor 3の細胞内局在、及びシグナル伝達に関与する機能ドメインの同定 : The cytoplasmic "linker region" in Toll-like receptor 3 controls receptor licalization and signaling; Toll-like receptor 3 ノサイボウナイキョクザイオヨビシグナルデンタツニカンヨスルキノウドメインノドウテイ.” Web. 23 Jan 2021.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

舟見 �. Toll-like receptor 3の細胞内局在、及びシグナル伝達に関与する機能ドメインの同定 : The cytoplasmic "linker region" in Toll-like receptor 3 controls receptor licalization and signaling; Toll-like receptor 3 ノサイボウナイキョクザイオヨビシグナルデンタツニカンヨスルキノウドメインノドウテイ. [Internet] [Thesis]. Nara Institute of Science and Technology / 奈良先端科学技術大学院大学; [cited 2021 Jan 23]. Available from: http://hdl.handle.net/10061/2831.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Council of Science Editors:

舟見 �. Toll-like receptor 3の細胞内局在、及びシグナル伝達に関与する機能ドメインの同定 : The cytoplasmic "linker region" in Toll-like receptor 3 controls receptor licalization and signaling; Toll-like receptor 3 ノサイボウナイキョクザイオヨビシグナルデンタツニカンヨスルキノウドメインノドウテイ. [Thesis]. Nara Institute of Science and Technology / 奈良先端科学技術大学院大学; Available from: http://hdl.handle.net/10061/2831

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

University of Rochester

5. Aggrey, Angela Akosua. A Novel Protective Role for Platelet-Mediated Immune Responses in Murine Experimental Cerebral Malaria.

Degree: PhD, 2013, University of Rochester

URL: http://hdl.handle.net/1802/27239

► Cerebral malaria is caused by complications from Plasmodium falciparum infection and claims hundreds of thousands of lives of young children in endemic countries annually. Platelets… (more)

Subjects/Keywords: Platelets; Innate Immunity, Malaria; Inflammation

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Aggrey, A. A. (2013). A Novel Protective Role for Platelet-Mediated Immune Responses in Murine Experimental Cerebral Malaria. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/27239

Chicago Manual of Style (16^th Edition):

Aggrey, Angela Akosua. “A Novel Protective Role for Platelet-Mediated Immune Responses in Murine Experimental Cerebral Malaria.” 2013. Doctoral Dissertation, University of Rochester. Accessed January 23, 2021. http://hdl.handle.net/1802/27239.

MLA Handbook (7^th Edition):

Aggrey, Angela Akosua. “A Novel Protective Role for Platelet-Mediated Immune Responses in Murine Experimental Cerebral Malaria.” 2013. Web. 23 Jan 2021.

Vancouver:

Aggrey AA. A Novel Protective Role for Platelet-Mediated Immune Responses in Murine Experimental Cerebral Malaria. [Internet] [Doctoral dissertation]. University of Rochester; 2013. [cited 2021 Jan 23]. Available from: http://hdl.handle.net/1802/27239.

Council of Science Editors:

Aggrey AA. A Novel Protective Role for Platelet-Mediated Immune Responses in Murine Experimental Cerebral Malaria. [Doctoral Dissertation]. University of Rochester; 2013. Available from: http://hdl.handle.net/1802/27239

6. Ramyar, Kasra Xerxes. Biochemical Characterization of Murine Qa-1.

Degree: 2014, Johns Hopkins University

URL: http://jhir.library.jhu.edu/handle/1774.2/37158

► Qa-1 is a member of the mouse MHC Ib family with roles in both the adaptive and innate arms of immunity. While it is presumed… (more)

Subjects/Keywords: Innate Immunity Immune Surveillance

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ramyar, K. X. (2014). Biochemical Characterization of Murine Qa-1. (Thesis). Johns Hopkins University. Retrieved from http://jhir.library.jhu.edu/handle/1774.2/37158

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Ramyar, Kasra Xerxes. “Biochemical Characterization of Murine Qa-1.” 2014. Thesis, Johns Hopkins University. Accessed January 23, 2021. http://jhir.library.jhu.edu/handle/1774.2/37158.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Ramyar, Kasra Xerxes. “Biochemical Characterization of Murine Qa-1.” 2014. Web. 23 Jan 2021.

Vancouver:

Ramyar KX. Biochemical Characterization of Murine Qa-1. [Internet] [Thesis]. Johns Hopkins University; 2014. [cited 2021 Jan 23]. Available from: http://jhir.library.jhu.edu/handle/1774.2/37158.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Ramyar KX. Biochemical Characterization of Murine Qa-1. [Thesis]. Johns Hopkins University; 2014. Available from: http://jhir.library.jhu.edu/handle/1774.2/37158

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Saskatchewan

7. Magiri, Royford Bundi 1983-. INNATE IMMUNE RESPONSES ACTIVATED BY THE ADJUVANT POLY [DI (SODIUM CARBOXYLATOETHYLPHENOXY)PHOSPHAZENE](PCEP) IN PIGS.

Degree: 2019, University of Saskatchewan

URL: http://hdl.handle.net/10388/12208

► ABSTRACT Adjuvants are critical components of vaccines because they enhance antigen-specific immune responses to protect against disease. However, the mechanisms of action (MOA) of most… (more)

▼ ABSTRACT Adjuvants are critical components of vaccines because they enhance antigen-specific immune responses to protect against disease. However, the mechanisms of action (MOA) of most adjuvants are not well understood and they particularly are under-investigated in large animal species including pigs and cattle. This knowledge gap may limit our ability to design effective vaccines for livestock. Understanding the mechanisms by which adjuvants mediate their effects could provide critical information on how innate immunity influences the development of adaptive immunity. Furthermore, knowledge on the MOA of adjuvants may inform vaccine the safety. In the present investigations, we studied the MOA of the experimental adjuvant polydi(sodium carboxylatoethylphenoxy)phosphazene (PCEP) in pigs. First, we administered PCEP by intradermal (i.d.) injection into pigs and assessed its impact on the expression of select immune response genes known as ‘adjuvant response genes’ over time. We observed that PCEP induced the expression of chemokine (C-C motif) ligand 2 (CCL-2), proinflammatory cytokine interleukin (IL)-6, IL-13 and macrophage scavenger receptor 1 (MSR1) genes at the site of injection. Next, we evaluated whether these gene expressions translate to protein transcription by accessing local and systemic production of cytokines after intradermal injection of PCEP into piglets and whether the cytokines produced induces recruitment of immune cells at the site of injection and in the draining lymph nodes. We observed that, at the site of injection, PCEP induced increased production of IL-1β and IL-13 cytokines, increased cellular infiltration of macrophages, T and B cells, and other leucocytes especially neutrophils as well as showing necrotic debris which might cause release of damage associated molecular patterns (DAMPs) and activate the inflammasome. In the draining lymph nodes, the cytokines IL-1β and IL-6 were elevated and there was increased leucocyte infiltration. No changes in cytokine levels were detected in the blood after PCEP injection indicating that the immunostimulatory effect of PCEP is local but not systemic. Because i.d. injection of PCEP induced signs of necrosis (cell death), we investigated whether reduction of the adjuvant dose reduced tissue damage without negatively impacting antigen-specific immune responses. We conducted two studies to address this issue. In the first study, we injected piglets i.d with varying doses of PCEP alone as follows: 500 μg, 100 μg, or 20 μg PCEP into piglets and evaluated the inflammatory responses. The four parameters evaluated were granuloma formation, lymphocytic infiltration, necrosis, and suppurative inflammation at the injection site and the draining lymph nodes over 14 days. When PCEP was injected alone, we observed that only 500 μg consistently induced significant necrosis and suppurative inflammation. However, the medium dose (100 μg) PCEP did induce significant skin granulomas and lymphocyte infiltration, where as the only significant response induced in… Advisors/Committee Members: Mutwiri, George, Wilson, Heather, Tikoo, Suresh, Huang, Yanyun, Singh, Baljit, Gomis, Susantha.

Subjects/Keywords: Innate immunity and adjuvants

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Magiri, R. B. 1. (2019). INNATE IMMUNE RESPONSES ACTIVATED BY THE ADJUVANT POLY [DI (SODIUM CARBOXYLATOETHYLPHENOXY)PHOSPHAZENE](PCEP) IN PIGS. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/12208

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Magiri, Royford Bundi 1983-. “INNATE IMMUNE RESPONSES ACTIVATED BY THE ADJUVANT POLY [DI (SODIUM CARBOXYLATOETHYLPHENOXY)PHOSPHAZENE](PCEP) IN PIGS.” 2019. Thesis, University of Saskatchewan. Accessed January 23, 2021. http://hdl.handle.net/10388/12208.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Magiri, Royford Bundi 1983-. “INNATE IMMUNE RESPONSES ACTIVATED BY THE ADJUVANT POLY [DI (SODIUM CARBOXYLATOETHYLPHENOXY)PHOSPHAZENE](PCEP) IN PIGS.” 2019. Web. 23 Jan 2021.

Vancouver:

Magiri RB1. INNATE IMMUNE RESPONSES ACTIVATED BY THE ADJUVANT POLY [DI (SODIUM CARBOXYLATOETHYLPHENOXY)PHOSPHAZENE](PCEP) IN PIGS. [Internet] [Thesis]. University of Saskatchewan; 2019. [cited 2021 Jan 23]. Available from: http://hdl.handle.net/10388/12208.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Magiri RB1. INNATE IMMUNE RESPONSES ACTIVATED BY THE ADJUVANT POLY [DI (SODIUM CARBOXYLATOETHYLPHENOXY)PHOSPHAZENE](PCEP) IN PIGS. [Thesis]. University of Saskatchewan; 2019. Available from: http://hdl.handle.net/10388/12208

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Penn State University

8. Dispenza, Melanie Claire. IMMUNOMODULATORY EFFECTS OF ISOTRETINOIN IN VIVO .

Degree: 2011, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/11965

► Acne is a common human ailment that can cause significant physical and psychological morbidity. Though it is thought to be partially caused by Propionibacterium acnes… (more)

▼ Acne is a common human ailment that can cause significant physical and psychological morbidity. Though it is thought to be partially caused by Propionibacterium acnes colonization, studies suggest that patients’ specific immune responses to P.acnes may play a larger role in acne than the pathogenicity of P.acnes itself. Isotretinoin, a pro-drug for retinoic acid, is the only agent that induces a permanent remission of acne, but the mechanism underlying its long-term efficacy is unknown. We hypothesized that modulation of the immune response to P.acnes is key to isotretinoin’s ability to induce long-term or permanent remissions of acne. In this Thesis, we show that acne patients’ monocytes express higher levels of TLR-2 and secrete more IL-1â, IL-6, IL-8, IL-10, and IL-12 in response to P. acnes than monocytes from normal volunteers. Isotretinoin therapy significantly decreases TLR-2 expression and inflammatory cytokine secretion by acne patients’ monocytes compared to baseline. These changes continue through 20 weeks of isotretinoin therapy and persist for at least six months after the cessation of therapy, indicating that modification of patients’ immune responses to P. acnes may represent a long-term mechanism by which isotretinoin can cure acne. Because the exogenous administration of retinoids causes severe side-effects including birth defects, studies characterizing the action of isotretinoin in humans in vivo are lacking. This is the first study to show that isotretinoin has immunomodulatory effects in acne patients in vivo. Findings from this study extend to other diseases for which isotretinoin is used as a therapy as well as inflammatory disorders characterized by TLR-2 over-expression. Advisors/Committee Members: Diane M Thiboutot, Dissertation Advisor/Co-Advisor, Diane M Thiboutot, Committee Chair/Co-Chair, Robert Harold Bonneau, Committee Member, Charles H Lang, Committee Member, Gary Alan Clawson, Committee Member, Stephen R Rannels, Committee Member.

Subjects/Keywords: monocytes; innate immunity; acne

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Dispenza, M. C. (2011). IMMUNOMODULATORY EFFECTS OF ISOTRETINOIN IN VIVO . (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/11965

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Dispenza, Melanie Claire. “IMMUNOMODULATORY EFFECTS OF ISOTRETINOIN IN VIVO .” 2011. Thesis, Penn State University. Accessed January 23, 2021. https://submit-etda.libraries.psu.edu/catalog/11965.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Dispenza, Melanie Claire. “IMMUNOMODULATORY EFFECTS OF ISOTRETINOIN IN VIVO .” 2011. Web. 23 Jan 2021.

Vancouver:

Dispenza MC. IMMUNOMODULATORY EFFECTS OF ISOTRETINOIN IN VIVO . [Internet] [Thesis]. Penn State University; 2011. [cited 2021 Jan 23]. Available from: https://submit-etda.libraries.psu.edu/catalog/11965.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Dispenza MC. IMMUNOMODULATORY EFFECTS OF ISOTRETINOIN IN VIVO . [Thesis]. Penn State University; 2011. Available from: https://submit-etda.libraries.psu.edu/catalog/11965

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Texas A&M University

9. Jiang, Shan. Plant Defense Signaling Mechanisms and Evolution.

Degree: PhD, Plant Pathology, 2015, Texas A&M University

URL: http://hdl.handle.net/1969.1/155604

► Plant innate immunity has been classified into two layers of defense systems. Nucleotide-binding domain leucine-rich repeat (NLR) protein complexes activated by pathogen effectors launches effector-triggered… (more)

▼ Plant innate immunity has been classified into two layers of defense systems. Nucleotide-binding domain leucine-rich repeat (NLR) protein complexes activated by pathogen effectors launches effector-triggered immunity (ETI). A forward genetic screen using the ETI marker gene WRKY46 promoter fused with a firefly luciferase gene (pWRKY46::LUC) as a reporter identified five ARABIDOPSIS GENES GOVERNING IMMUNE GENE EXPRESSION (aggie) mutants, named as aggie4-8. Though with elevated pWRKY46::LUC activity, aggie4 showed enhanced resistance to avirulent bacterial infections, yet delayed hypersensitive response (HR), while aggie5 exhibited compromised disease resistance and delayed HR. Map-based cloning coupled with next generation sequencing (NGS) suggests that causal mutations of aggie4 and aggie5 locate in different regions of chromosome 5. In addition, pWRKY46::LUC activity is elevated in aggie6 and aggie7, while suppressed in aggie8. Perception of microbe-associated molecular patterns (MAMPs) by pattern recognition receptors (PRRs) triggers another tier of innate immunity, termed as pattern-triggered immunity (PTI). The Arabidopsis SOMATIC EMBRYOGENESIS RECEPTOR KINASE (SERK) family plays important roles in plant defense responses. It remains unknown how SERK members have evolved. Here, three SERK homologs, Pp1s35_219V6.1, Pp1s96_90V6.1 and Pp1s118_79V6.1 were identified in P. Patens with 60%-80% amino acid identify to AtSERKs and were named as PpSERK1.1, PpSERK1.2 and PpSERK2 respectively. In vitro kinase assay revealed that PpSERK1.1 and PpSERK1.2, but not PpSERK2, possess strong kinase activity. Functional complementation analysis suggested that PpSERK1.1 and PpSERK1.2 but not PpSERK2 regulate FLS2-mediated plant defense, and PpSERK1.2 but not PpSERK1.1 also regulates cell death in Arabidopsis. PTI induces a rapid and profound transcriptional reprograming via concerted actions of specific transcription factors and general transcription machinery. Arabidopsis SH4-related 3 (ASR3), a plant specific trihelix family of transcription factors, is rapidly phosphorylated by MPK4 at Threonine 189 residue upon multiple MAMP treatments but not upon elicitation of ETI. Genetic and biochemical data suggests that phosphorylation of ASR3 enhances its DNA binding activity to suppress immune genes expression. Importantly, the asr3 mutant shows higher immune gene activation and enhanced disease resistance, while transgenic plants overexpressing ASR3 exhibit compromised PTI responses. This study reveals that ASR3 functions as a transcription repressor regulated by MPK4 to fine-tune plant defense. Advisors/Committee Members: Shan, Libo (advisor), He, Ping (committee member), Kenerley, Charles (committee member), Figueiredo, Paul de (committee member).

Subjects/Keywords: Plant defense; innate immunity; evolution

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Jiang, S. (2015). Plant Defense Signaling Mechanisms and Evolution. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/155604

Chicago Manual of Style (16^th Edition):

Jiang, Shan. “Plant Defense Signaling Mechanisms and Evolution.” 2015. Doctoral Dissertation, Texas A&M University. Accessed January 23, 2021. http://hdl.handle.net/1969.1/155604.

MLA Handbook (7^th Edition):

Jiang, Shan. “Plant Defense Signaling Mechanisms and Evolution.” 2015. Web. 23 Jan 2021.

Vancouver:

Jiang S. Plant Defense Signaling Mechanisms and Evolution. [Internet] [Doctoral dissertation]. Texas A&M University; 2015. [cited 2021 Jan 23]. Available from: http://hdl.handle.net/1969.1/155604.

Council of Science Editors:

Jiang S. Plant Defense Signaling Mechanisms and Evolution. [Doctoral Dissertation]. Texas A&M University; 2015. Available from: http://hdl.handle.net/1969.1/155604

University of Texas Southwestern Medical Center

10. Owen, David Matthew. Hepatitis C Virus Entry into Hepatocytes and Engagement of Innate Immune Defenses.

Degree: 2011, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/874

► Hepatitis C virus (HCV) infection is a major cause of liver disease and a global health problem with inadequate treatment options. An improved understanding of… (more)

▼ Hepatitis C virus (HCV) infection is a major cause of liver disease and a global health problem with inadequate treatment options. An improved understanding of how HCV exploits and subverts host factors to establish infection should yield potential targets for therapy. This study uses a recently developed cell culture model of HCV infection to examine HCV entry and engagement of innate immune defenses. HCV associates with host apolipoproteins and enters hepatocytes through complex processes involving some combination of CD81, claudin-I, occludin, and scavenger receptor BI. Here I show that HCV forms a complex with very low density lipoprotein (VLDL) within infected hepatocytes and uses this association to support infection through the low density lipoprotein receptor (LDL-R). Blocking experiments demonstrate that beta-VLDL and apolipoprotein E (apoE) can compete with HCV for entry. Knockdown of the LDL-R by treatment with 25-hydroxycholesterol or siRNA ablated ligand uptake and reduced HCV infection of cells, whereas infection was rescued upon cell ectopic LDL-R expression. Analyses of gradient-fractionated HCV demonstrate that apoE is associated with HCV virions exhibiting peak infectivity and dependence upon the LDL-R for cell entry. These results define the LDL-R as a cooperative HCV co-receptor that supports viral entry and infectivity through interaction with apoE ligand present in an infectious HCV/lipoprotein complex comprising the virion. Furthermore, upon entry HCV induces an initial transient activation of interferon regulatory factor-3 (IRF3) which is dependent on retinoic acid inducible gene I (RIG-I) and interferon-beta promoter stimulator-1 (IPS-1). This activation produces an antiviral activity which inhibits HCV entry and replication. HCV NS3/4A protease activity blocks this activation within 48 hours. At later time points post infection HCV activates NF-kappaB in a RIG-I independent manner leading to inflammatory cytokine production. These studies identify 3 potential targets for future HCV therapy: 1) alteration of HCV-lipoprotein interaction to disrupt entry, 2) blockade of NS3/4A protease activity to restore innate antiviral response, and 3) modulation of HCV induced NF-kappaB signaling to downregulate chronic inflammation. Advisors/Committee Members: Gale, Michael, Jr..

Subjects/Keywords: RNA Helicases; Immunity, Innate; Hepacivirus

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Owen, D. M. (2011). Hepatitis C Virus Entry into Hepatocytes and Engagement of Innate Immune Defenses. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/874

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Owen, David Matthew. “Hepatitis C Virus Entry into Hepatocytes and Engagement of Innate Immune Defenses.” 2011. Thesis, University of Texas Southwestern Medical Center. Accessed January 23, 2021. http://hdl.handle.net/2152.5/874.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Owen, David Matthew. “Hepatitis C Virus Entry into Hepatocytes and Engagement of Innate Immune Defenses.” 2011. Web. 23 Jan 2021.

Vancouver:

Owen DM. Hepatitis C Virus Entry into Hepatocytes and Engagement of Innate Immune Defenses. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2011. [cited 2021 Jan 23]. Available from: http://hdl.handle.net/2152.5/874.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Owen DM. Hepatitis C Virus Entry into Hepatocytes and Engagement of Innate Immune Defenses. [Thesis]. University of Texas Southwestern Medical Center; 2011. Available from: http://hdl.handle.net/2152.5/874

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Guelph

11. Berghuis, Lesley. Stimulating innate immunity in feedlot cattle: strategies to induce tracheal antimicrobial peptide gene expression.

Degree: MS, Department of Pathobiology, 2014, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7762

► Tracheal antimicrobial peptide (TAP) is a β-defensin with microbicidal activity against bacterial pathogens causing bovine respiratory disease. Lipopolysaccharide stimulates TAP gene expression, with maximal effect… (more)

Subjects/Keywords: Innate immunity; feedlot cattle

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Berghuis, L. (2014). Stimulating innate immunity in feedlot cattle: strategies to induce tracheal antimicrobial peptide gene expression. (Masters Thesis). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7762

Chicago Manual of Style (16^th Edition):

Berghuis, Lesley. “Stimulating innate immunity in feedlot cattle: strategies to induce tracheal antimicrobial peptide gene expression.” 2014. Masters Thesis, University of Guelph. Accessed January 23, 2021. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7762.

MLA Handbook (7^th Edition):

Berghuis, Lesley. “Stimulating innate immunity in feedlot cattle: strategies to induce tracheal antimicrobial peptide gene expression.” 2014. Web. 23 Jan 2021.

Vancouver:

Berghuis L. Stimulating innate immunity in feedlot cattle: strategies to induce tracheal antimicrobial peptide gene expression. [Internet] [Masters thesis]. University of Guelph; 2014. [cited 2021 Jan 23]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7762.

Council of Science Editors:

Berghuis L. Stimulating innate immunity in feedlot cattle: strategies to induce tracheal antimicrobial peptide gene expression. [Masters Thesis]. University of Guelph; 2014. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7762

University of Guelph

12. Misk, Ehab. Pathogenesis and Distribution of Spring Viremia of Carp Virus (SVCV) in Ontario.

Degree: PhD, Department of Pathobiology, 2016, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/9687

► Spring viremia of carp virus (SVCV), an OIE reportable rhabdovirus and fish pathogen, was identified in Canada in 2006 in Hamilton Harbour but has not… (more)

▼ Spring viremia of carp virus (SVCV), an OIE reportable rhabdovirus and fish pathogen, was identified in Canada in 2006 in Hamilton Harbour but has not been reported subsequently. SVCV can have a significant impact on cyprinids, and so the susceptibility of three baitfish species (emerald shiner Notropis atherinoides, fathead minnow Pimpheles promelas, white sucker Catostomus commersonii from the order Cypriniformes was assessed using experimental infection. Millions of baitfish are moved around the province to support the sports fishing industry, and this represents a risk for spread of the virus. Emerald shiner, fathead minnow and koi (43, 53, and 33% mortality, respectively) were highly susceptible, but white sucker or rainbow trout (12.5 and 0% mortality), were not. Infection was confirmed by virus isolation and RT-qPCR and SVCV was immunolocalized in association with histological lesions using immunohistochemistry. A one-step reverse transcription quantitative PCR (RT-qPCR) was adapted and used retrospectively to test samples collected by the Ontario Ministry of Natural Resources for surveillance from 2008 to 2012. A total of 1432 fish from 35 water bodies in Ontario were examined using RT-qPCR, but no additional fish were identified with SVCV. Finally, the pathogenesis of the Rhabdovirus-host interaction at the gill epithelium was investigated using the RTgill-W1 cells. The cell line was pretreated with UV-inactivated (killed) VHSV and recombinant FliC and then infected with viral hemorrhagic septicemia virus (VHSV). The viral load and gene expression was investigated 1, 3, and 6 d post infection (PI) with qPCR. In addition, the transcriptome response of RTgill-W1 cells at 36 h post-treatment with SVCV, VHSV, UV-inactivated VHSV and FliC were tested using microarray and RT-qPCR. Pretreatment of RTgill-W1 cells with killed VSHV induced a reduction in viral load (nucleoprotein copy number by RT-qPCR) after infection. Transcription profiles in VHSV- and SVCV-infected or killed VHSV and FliC pretreated RTgill-W1 cells 36 h post-exposure detected 24, 22, 123 and 190 differentially expressed probes, which contained several important gene candidates with a potentially key role in innate immunity to rhabdovirus infection in gill epithelium. Advisors/Committee Members: Lumsden, John (advisor).

Subjects/Keywords: Innate immunity; SVCV; Microarray

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Misk, E. (2016). Pathogenesis and Distribution of Spring Viremia of Carp Virus (SVCV) in Ontario. (Doctoral Dissertation). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/9687

Chicago Manual of Style (16^th Edition):

Misk, Ehab. “Pathogenesis and Distribution of Spring Viremia of Carp Virus (SVCV) in Ontario.” 2016. Doctoral Dissertation, University of Guelph. Accessed January 23, 2021. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/9687.

MLA Handbook (7^th Edition):

Misk, Ehab. “Pathogenesis and Distribution of Spring Viremia of Carp Virus (SVCV) in Ontario.” 2016. Web. 23 Jan 2021.

Vancouver:

Misk E. Pathogenesis and Distribution of Spring Viremia of Carp Virus (SVCV) in Ontario. [Internet] [Doctoral dissertation]. University of Guelph; 2016. [cited 2021 Jan 23]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/9687.

Council of Science Editors:

Misk E. Pathogenesis and Distribution of Spring Viremia of Carp Virus (SVCV) in Ontario. [Doctoral Dissertation]. University of Guelph; 2016. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/9687

University of Miami

13. Ma, Zhe. DDX24 Negatively Regulates Cytosolic RNA Mediated Innate Immune Signaling.

Degree: PhD, Cancer Biology (Medicine), 2013, University of Miami

URL: https://scholarlyrepository.miami.edu/oa_dissertations/1098

► Innate immunity is characterized by production of type I interferon which is necessary for the stimulation of effective anti-viral host defense. Upon recognition of cytosol… (more)

Subjects/Keywords: Innate immunity: RIG-I

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ma, Z. (2013). DDX24 Negatively Regulates Cytosolic RNA Mediated Innate Immune Signaling. (Doctoral Dissertation). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_dissertations/1098

Chicago Manual of Style (16^th Edition):

Ma, Zhe. “DDX24 Negatively Regulates Cytosolic RNA Mediated Innate Immune Signaling.” 2013. Doctoral Dissertation, University of Miami. Accessed January 23, 2021. https://scholarlyrepository.miami.edu/oa_dissertations/1098.

MLA Handbook (7^th Edition):

Ma, Zhe. “DDX24 Negatively Regulates Cytosolic RNA Mediated Innate Immune Signaling.” 2013. Web. 23 Jan 2021.

Vancouver:

Ma Z. DDX24 Negatively Regulates Cytosolic RNA Mediated Innate Immune Signaling. [Internet] [Doctoral dissertation]. University of Miami; 2013. [cited 2021 Jan 23]. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/1098.

Council of Science Editors:

Ma Z. DDX24 Negatively Regulates Cytosolic RNA Mediated Innate Immune Signaling. [Doctoral Dissertation]. University of Miami; 2013. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/1098

University of Manitoba

14. Dick, Kevin James. Mutational analysis of the dsRNA binding domain of Vaccinia Virus E3 protein.

Degree: Medical Microbiology, 2011, University of Manitoba

URL: http://hdl.handle.net/1993/4852

► Vaccinia virus E3 protein is known to bind double-stranded RNA and mediate interferon resistance. Alanine scanning mutagenesis was performed on its dsRNA binding domain, sufficient… (more)

Subjects/Keywords: Virology; Innate Immunity; Poxvirus

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Dick, K. J. (2011). Mutational analysis of the dsRNA binding domain of Vaccinia Virus E3 protein. (Masters Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/4852

Chicago Manual of Style (16^th Edition):

Dick, Kevin James. “Mutational analysis of the dsRNA binding domain of Vaccinia Virus E3 protein.” 2011. Masters Thesis, University of Manitoba. Accessed January 23, 2021. http://hdl.handle.net/1993/4852.

MLA Handbook (7^th Edition):

Dick, Kevin James. “Mutational analysis of the dsRNA binding domain of Vaccinia Virus E3 protein.” 2011. Web. 23 Jan 2021.

Vancouver:

Dick KJ. Mutational analysis of the dsRNA binding domain of Vaccinia Virus E3 protein. [Internet] [Masters thesis]. University of Manitoba; 2011. [cited 2021 Jan 23]. Available from: http://hdl.handle.net/1993/4852.

Council of Science Editors:

Dick KJ. Mutational analysis of the dsRNA binding domain of Vaccinia Virus E3 protein. [Masters Thesis]. University of Manitoba; 2011. Available from: http://hdl.handle.net/1993/4852

University of Cambridge

15. Mears, Harriet Victoria. On the expression, function and regulation of the murine Ifit family of antiviral RNA-binding proteins.

Degree: PhD, 2020, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/300608

► IFIT proteins are highly expressed as part of the cell-intrinsic immune response following viral infection. In humans, IFIT1 inhibits translation at the initiation stage by… (more)

▼ IFIT proteins are highly expressed as part of the cell-intrinsic immune response following viral infection. In humans, IFIT1 inhibits translation at the initiation stage by binding directly to the 5' terminus of foreign RNA, precluding the recruitment of the cap-binding translation initiation factor complex eIF4F. IFIT1 is highly specific for ‘non-self’ cap0 RNA, which lacks methylation on the first and second cap-proximal nucleotides, but at high concentrations may also restrict ‘self’ cap1 translation. Knock-out mouse models have been extensively used to study IFIT antiviral activity and, more recently, vaccines based on the antiviral activity of IFIT1 have been trialled for efficacy in mice. However, it is becoming clear that there are differences in murine and human IFIT function and regulation, which impacts the interpretation of these models. Mice lack a true orthologue of IFIT1 and instead the closely related Ifit1b has been duplicated twice, yielding three paralogues: Ifit1, Ifit1b and Ifit1c. Murine Ifit1, like human IFIT1, can bind to cap0 RNA and inhibit its translation, but lacks cap1 binding activity. Ifit1b and Ifit1c are closely related to Ifit1 and share many of the residues critical for RNA-binding, but their precise functions are unknown. In this thesis, the expression of the entire murine Ifit family was examined in different mouse cell lines, validating expression of Ifit1b and Ifit1c following interferon stimulation. The murine Ifit family was then recombinantly expressed and purified, allowing biochemical characterisation. It was discovered that Ifit1b, a previously uncharacterised protein, preferentially inhibited the translation of cap1 mRNA, while cap0 and cap2 mRNAs were inhibited to a much lesser extent. Specific cap1 binding allows Ifit1b to inhibit a proportion of cellular translation and block translation of murine hepatitis virus, a cap1 coronavirus. However, both Ifit1 and Ifit1b were incapable of inhibiting translation from a more structured Zika virus reporter mRNA. The same reporter was effectively inhibited by human IFIT1, highlighting a key difference between the activities of human and murine IFIT proteins. IFIT proteins are known to form both homo- and hetero-oligomers, but the functional significance of these interactions is unclear. Here, interaction between human IFIT1 and IFIT3 was shown to increase the stability of both proteins and stimulate translation inhibition by IFIT1. IFIT1 and IFIT3 interacted via a C-terminal YxxxL motif, and disruption of this motif in either protein abolished the cofactor activity of IFIT3, both in vitro and in cells. In mice, Ifit3 is truncated and lacks the YxxxL motif, thus precluding interaction with murine Ifit1. However, this motif is maintained in Ifit1, Ifit1b and Ifit1c, which were found to interact with one-another in vitro. Interaction between murine Ifit proteins increased their stability and Ifit1c enhanced translation inhibition by Ifit1 and Ifit1b in vitro, thereby acting analogously to human IFIT3. Together this work…

Subjects/Keywords: Innate immunity; Interferon; Antiviral response

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mears, H. V. (2020). On the expression, function and regulation of the murine Ifit family of antiviral RNA-binding proteins. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/300608

Chicago Manual of Style (16^th Edition):

Mears, Harriet Victoria. “On the expression, function and regulation of the murine Ifit family of antiviral RNA-binding proteins.” 2020. Doctoral Dissertation, University of Cambridge. Accessed January 23, 2021. https://www.repository.cam.ac.uk/handle/1810/300608.

MLA Handbook (7^th Edition):

Mears, Harriet Victoria. “On the expression, function and regulation of the murine Ifit family of antiviral RNA-binding proteins.” 2020. Web. 23 Jan 2021.

Vancouver:

Mears HV. On the expression, function and regulation of the murine Ifit family of antiviral RNA-binding proteins. [Internet] [Doctoral dissertation]. University of Cambridge; 2020. [cited 2021 Jan 23]. Available from: https://www.repository.cam.ac.uk/handle/1810/300608.

Council of Science Editors:

Mears HV. On the expression, function and regulation of the murine Ifit family of antiviral RNA-binding proteins. [Doctoral Dissertation]. University of Cambridge; 2020. Available from: https://www.repository.cam.ac.uk/handle/1810/300608

University of Toronto

16. Gaudet, Ryan Gilbert. TIFA-Mediated Innate Immune Recognition of the Bacterial Metabolite HBP and its Role in Host Defense.

Degree: PhD, 2016, University of Toronto

URL: http://hdl.handle.net/1807/76423

► Host recognition of pathogen-associated molecular patterns (PAMPs) initiates an innate immune response that is critical for pathogen elimination and engagement of adaptive immunity. Here I… (more)

▼ Host recognition of pathogen-associated molecular patterns (PAMPs) initiates an innate immune response that is critical for pathogen elimination and engagement of adaptive immunity. Here I show that mammalian immune and nonimmune cells can detect and respond to the bacterial derived monosaccharide heptose-1,7-bisphosphate (HBP). A metabolic intermediate in lipopolysaccharide (LPS) biosynthesis, HBP is highly conserved in Gram-negative bacteria, yet absent from eukaryotic cells. Detection of HBP within the host cytosol activated the NF-ÎşB pathway in vitro, and induced innate and adaptive immune responses in vivo. HBP-induced signaling was independent of known pattern recognition receptor pathways. Therefore, I used a genome-wide RNAi screen to uncover an innate immune signaling axis, mediated by the TRAFinteracting protein with forkhead-associated domain (TIFA). Contamination of the host cytosol with HBP induced TIFA phosphorylation-dependent oligomerization and concomitant activation of the ubiquitin ligase TRAF6. In addition to recognizing HBP released upon bacterial lysis extracellularly or within the phagolysosome, I show that TIFA is an innate immune sensor for cytosol-invasive Gram-negative bacteria, as invasive Shigella flexneri, or a vacuole-escaping Salmonella mutant, released the HBP during cytosolic growth, triggering a sustained wave of TIFA activation that followed transient activation of the NOD1 pathway. Bacterial growth within the cytosol was essential for HBP release and concomitant TIFA activation, since prolonged infection with wild-type Shigella, but not metabolically attenuated invasive mutants, triggered TIFA-oligomerization and signaling to drive a massive NF-ÎşB response from human epithelial cells. My findings identify HBP as a novel PAMP, and as a corollary, TIFA as a new innate immune signalling effector that is the keystone of an immunosurveillance system that detects Gram-negative bacterial infection, and which escalates the immune response to invasive bacteria that exploit the host cytosol as a niche for growth and replication. Advisors/Committee Members: Gray-Owen, Scott D, Molecular and Medical Genetics.

Subjects/Keywords: Infection; Innate Immunity; 0982

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Gaudet, R. G. (2016). TIFA-Mediated Innate Immune Recognition of the Bacterial Metabolite HBP and its Role in Host Defense. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/76423

Chicago Manual of Style (16^th Edition):

Gaudet, Ryan Gilbert. “TIFA-Mediated Innate Immune Recognition of the Bacterial Metabolite HBP and its Role in Host Defense.” 2016. Doctoral Dissertation, University of Toronto. Accessed January 23, 2021. http://hdl.handle.net/1807/76423.

MLA Handbook (7^th Edition):

Gaudet, Ryan Gilbert. “TIFA-Mediated Innate Immune Recognition of the Bacterial Metabolite HBP and its Role in Host Defense.” 2016. Web. 23 Jan 2021.

Vancouver:

Gaudet RG. TIFA-Mediated Innate Immune Recognition of the Bacterial Metabolite HBP and its Role in Host Defense. [Internet] [Doctoral dissertation]. University of Toronto; 2016. [cited 2021 Jan 23]. Available from: http://hdl.handle.net/1807/76423.

Council of Science Editors:

Gaudet RG. TIFA-Mediated Innate Immune Recognition of the Bacterial Metabolite HBP and its Role in Host Defense. [Doctoral Dissertation]. University of Toronto; 2016. Available from: http://hdl.handle.net/1807/76423

University of Hawaii – Manoa

17. Yang, Baojun. Cellular response of insect cells to virus infection.

Degree: 2015, University of Hawaii – Manoa

URL: http://hdl.handle.net/10125/100551

►

Ph.D. University of Hawaii at Manoa 2014.

RNA interference (RNAi) is the dsRNA-triggered gene regulatory mechanism that is evolutionally conserved in most eukaryotic cells. It… (more)

▼

Ph.D. University of Hawaii at Manoa 2014.

RNA interference (RNAi) is the dsRNA-triggered gene regulatory mechanism that is evolutionally conserved in most eukaryotic cells. It has been widely used as a powerful tool for functional genomics in various organisms. In flies, mosquitoes or other insect cells, gene functional analysis by RNAi is usually performed through introduced dsRNAs that are synthesized by in vitro transcription. RNAi serves as an important innate immunity against viruses in plants and invertebrates. It has recently been shown that Aedes albopictus mosquito C6/36 cells, commonly used for arbovirus propagation, possess an impaired RNAi pathway. In this study, we developed in vitro Dicer assay using extracts prepared from mosquito cells. Our results confirmed the inability of C6/36 cells to process dsRNAs into siRNAs, which is consistent with the loss-of-function of Dcr-2 due to a frameshift mutation. However, such a defect could not be complemented by introduction of Drosophila Dicer-2. To evaluate the RNAi-based antiviral mechanism in C6/36 cells, we analyzed the replication of a mutant Nodamura virus (NoV) genomic RNA1 of which viral RNAi suppressor B2 is not expressed (NoVR1ΔB2) and cannot accumulate to a detectable level in RNAi-competent cells. In C6/36 cells, the defective RNAi gives rise to complete restoration of NoVR1ΔB2 replication, suggesting that RNAi is the primary antiviral immunity in mosquito cells. At present, dsRNA, as the trigger of the antiviral RNAi pathway in invertebrate and plants, is the major efficiency limitation factor in RNAi. In this study, a plasmid-based system was developed to express dsRNA intracellular from a DNA cassette containing two convergent T7 promoters in Drosophila S2 cells. Efficient knockdown of a transiently expressed reporter gene or an endogenous gene can be achieved by dsRNA expressed from the system. A random cDNA library was constructed in the dsRNA expression cassette and initial screening led to identification of two host factors that are involved in antiviral response in Drosophila S2 cells. The plasmid-based dsRNA expression system provides an alternative tool for functional genomics in Drosophila and other insect cells.

Subjects/Keywords: Antiviral; dsRNA; RNAi; Innate Immunity

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Yang, B. (2015). Cellular response of insect cells to virus infection. (Thesis). University of Hawaii – Manoa. Retrieved from http://hdl.handle.net/10125/100551

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Yang, Baojun. “Cellular response of insect cells to virus infection.” 2015. Thesis, University of Hawaii – Manoa. Accessed January 23, 2021. http://hdl.handle.net/10125/100551.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Yang, Baojun. “Cellular response of insect cells to virus infection.” 2015. Web. 23 Jan 2021.

Vancouver:

Yang B. Cellular response of insect cells to virus infection. [Internet] [Thesis]. University of Hawaii – Manoa; 2015. [cited 2021 Jan 23]. Available from: http://hdl.handle.net/10125/100551.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Yang B. Cellular response of insect cells to virus infection. [Thesis]. University of Hawaii – Manoa; 2015. Available from: http://hdl.handle.net/10125/100551

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Louisiana State University

18. Guo, Xunyang. RNAi-mediated Antiviral Immunity in Caenorhabditis elegans.

Degree: PhD, 2013, Louisiana State University

URL: etd-11082013-124052 ; https://digitalcommons.lsu.edu/gradschool_dissertations/3132

► Viruses are tiny intracellular parasites that often cause devastating diseases on cellular organisms. To suppress viral infection, cellular organisms have evolved a wide spectrum of… (more)

▼ Viruses are tiny intracellular parasites that often cause devastating diseases on cellular organisms. To suppress viral infection, cellular organisms have evolved a wide spectrum of antiviral defense mechanisms. Antiviral RNA interference (RNAi) is one of the antiviral mechanisms conserved in eukaryotes. During antiviral RNAi, the destruction of invading viral RNAs is mediated by small interfering RNAs derived from the viral replication complex, in the form of double-stranded RNA (dsRNA). Because of its sequence-specific nature, antiviral RNAi can also target host homologous transcripts, for instance leading to disease syndromes in plants. As a counter-defense mechanism, many viruses produce RNAi suppressors that suppress RNAi through distinct mechanisms. So far, RNAi-mediated virus-host interactions have remained largely unexplored in the nematode worms which are known to have a unique RNAi gene constitution. As a result, whether virus-derived siRNAs (viRNAs) are able to direct worm gene silencing, whether heterologous viral suppressors are still functional in nematode worms and how the worm-specific RNAi genes contribute to antiviral RNAi remain open questions. In this thesis I describe my exploration of several aspects of RNAi-mediated virus-host interaction in the nematode Caenorhabditis elegans. Through the study of virus-induced gene silencing in C. elegans I found that viRNAs can target and silence host genes. This is the first demonstration that viRNAs have the potential to silence host gene expression in the animal kingdom. Since certain viral suppressors that inhibit viRNA function without a size reference become resistant to RNAi but some suppressors that specifically suppress the function of 21-nucleotide (nt) viRNAs still sensitive to RNAi, I conclude that 21-nt viRNAs do not play a major role in worm antiviral RNAi. My study on the function of a worm-specific RNAi gene, called rsd-2 (RNAi spreading defective 2), suggested that antiviral RNAi in C. elegans can be initiated in the absence of a dsRNA binding protein, which is in sharp contrast to that in plant and insect systems. Through functional domain swap and viRNA profiling, I found that RIG-I-like RNA helicases contribute to worm antiviral RNAi through distinct mechanisms with one of them contributing to virus detection.

Subjects/Keywords: RNAi; innate immunity; C.elegans

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Guo, X. (2013). RNAi-mediated Antiviral Immunity in Caenorhabditis elegans. (Doctoral Dissertation). Louisiana State University. Retrieved from etd-11082013-124052 ; https://digitalcommons.lsu.edu/gradschool_dissertations/3132

Chicago Manual of Style (16^th Edition):

Guo, Xunyang. “RNAi-mediated Antiviral Immunity in Caenorhabditis elegans.” 2013. Doctoral Dissertation, Louisiana State University. Accessed January 23, 2021. etd-11082013-124052 ; https://digitalcommons.lsu.edu/gradschool_dissertations/3132.

MLA Handbook (7^th Edition):

Guo, Xunyang. “RNAi-mediated Antiviral Immunity in Caenorhabditis elegans.” 2013. Web. 23 Jan 2021.

Vancouver:

Guo X. RNAi-mediated Antiviral Immunity in Caenorhabditis elegans. [Internet] [Doctoral dissertation]. Louisiana State University; 2013. [cited 2021 Jan 23]. Available from: etd-11082013-124052 ; https://digitalcommons.lsu.edu/gradschool_dissertations/3132.

Council of Science Editors:

Guo X. RNAi-mediated Antiviral Immunity in Caenorhabditis elegans. [Doctoral Dissertation]. Louisiana State University; 2013. Available from: etd-11082013-124052 ; https://digitalcommons.lsu.edu/gradschool_dissertations/3132

University of Kentucky

19. Banerjee, Meenakshi. PLATELET ENDOCYTOSIS: ROLES IN HEMOSTASIS AND INNATE IMMUNITY.

Degree: 2017, University of Kentucky

URL: https://uknowledge.uky.edu/biochem_etds/32

► Endocytosis is key to fibrinogen (Fg) uptake, receptor trafficking of integrins (αIIbβ3, αvβ3) and purinergic receptors (P2Y1, P2Y12), and thereby for normal platelet function. However,… (more)

▼ Endocytosis is key to fibrinogen (Fg) uptake, receptor trafficking of integrins (αIIbβ3, αvβ3) and purinergic receptors (P2Y1, P2Y12), and thereby for normal platelet function. However, platelet endocytosis could potentially be critical for actively sensing changes in vascular micro-environments and responding accordingly to what is being taken up. This is a more dynamic view of platelets as active surveyors of the vasculature; extending the importance of platelet endocytosis beyond granule biogenesis and perhaps even hemostasis. The mechanistic underpinnings of endocytosis, its importance in platelets, and the molecular machinery required and possible trafficking routes are however understudied, in part due to a lack of experimental tools. The work presented here, puts forth new players that regulate platelet endocytosis and mediate cargo loading and hemostasis as well as provides a novel mechanistic understanding of how endocytosis allows platelets to act as immune cells and become the first responders to pathogens in the vasculature. Previously we showed the importance of ADP-ribosylation factor 6 (Arf6), which regulates αIIbβ3-mediated Fg uptake/storage and affects acute platelet functions e.g., clot retraction and spreading. To further identify elements of this endocytic machinery, we examined the role of a vesicle-residing Soluble N-ethylmaleimide Factor Attachment Protein Receptor (v-SNARE) called Cellubrevin/Vesicle Associated Membrane Protein-3 (VAMP-3) in platelet function. VAMP-3 KO mice had less platelet-associated Fg, indicating a defect in Fg uptake/storage. Loss of VAMP-3 led to defective uptake of fluorescently-tagged Fg and low-molecular dextran in platelets though it had a greater negative effect on receptor-mediated Fg uptake than on the fluid-phase marker uptake. Additionally, we followed the time-dependent trafficking of Fg and dextran into platelets using 3D-Structured Illumination Microscopy. Wild-type platelets endocytosed both cargo but quickly sorted them into distinct compartments with partial overlap occurring only at early time points. Sorting was unaffected in VAMP-3KO platelets. VAMP-3 loss did affect some acute platelet functions leading to enhanced spreading on Fg and faster clot retraction compared to wild-type. Additionally, the rate of JAK2 phosphorylation, initiated through the thrombopoietin receptor (TPOR/Mpl) activation, was affected in VAMP-3 KO platelets. The idea that platelets can act as immune cells and contribute to innate immunity has been increasingly gaining ground. Groups have correlated thrombocytopenia with clinical outcomes of viremia and bacteremia. Chronic viral infections, e.g., HIV-1, severely increase the risk of acute myocardial infarction (MI), possibly via some level of platelet activation, contributing to increased thrombotic potential. Platelets do endocytose viruses and bacteria, but the molecular machinery is ill-defined. In nucleated cells, responses to HIV-1 are mediated by virus phagocytosis/endocytosis, degradation to release Toll-like Receptor…

Subjects/Keywords: platelets; endocytosis; innate immunity; Biochemistry

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Banerjee, M. (2017). PLATELET ENDOCYTOSIS: ROLES IN HEMOSTASIS AND INNATE IMMUNITY. (Doctoral Dissertation). University of Kentucky. Retrieved from https://uknowledge.uky.edu/biochem_etds/32

Chicago Manual of Style (16^th Edition):

Banerjee, Meenakshi. “PLATELET ENDOCYTOSIS: ROLES IN HEMOSTASIS AND INNATE IMMUNITY.” 2017. Doctoral Dissertation, University of Kentucky. Accessed January 23, 2021. https://uknowledge.uky.edu/biochem_etds/32.

MLA Handbook (7^th Edition):

Banerjee, Meenakshi. “PLATELET ENDOCYTOSIS: ROLES IN HEMOSTASIS AND INNATE IMMUNITY.” 2017. Web. 23 Jan 2021.

Vancouver:

Banerjee M. PLATELET ENDOCYTOSIS: ROLES IN HEMOSTASIS AND INNATE IMMUNITY. [Internet] [Doctoral dissertation]. University of Kentucky; 2017. [cited 2021 Jan 23]. Available from: https://uknowledge.uky.edu/biochem_etds/32.

Council of Science Editors:

Banerjee M. PLATELET ENDOCYTOSIS: ROLES IN HEMOSTASIS AND INNATE IMMUNITY. [Doctoral Dissertation]. University of Kentucky; 2017. Available from: https://uknowledge.uky.edu/biochem_etds/32

University of Illinois – Urbana-Champaign

20. Gates-Tanzer, Lauren Taylor. Characterization of the anti-type I interferon effects of the cellular flice-like inhibitory protein (CFLIP).

Degree: PhD, Microbiology, 2018, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/101696

► The cellular FLICE-like inhibitory protein (cFLIP) is well known as a major immunomodulatory protein. Various works have described its role in major cellular pathways such… (more)

▼ The cellular FLICE-like inhibitory protein (cFLIP) is well known as a major immunomodulatory protein. Various works have described its role in major cellular pathways such as apoptosis, autophagy, necroptosis, NF-KB regulation and more recently, modulation of interferon responses. Interferon alpha (IFNa) and interferon beta (IFNb) are in the class of type I IFN and are critical as the first line of defense against viral infection. Interestingly, these IFNs also maintain roles apart from viral infection including participating in the pathophysiology of tumor biology and autoimmunity. Previous studies found that cFLIPL could inhibit IFNb production. My work demonstrated that this was by inhibiting the major transcription factor for IFNb expression, interferon regulatory factor 3 (IRF3). Mutational analysis revealed that the CLD within the C-terminus of cFLIPL is responsible for inhibiting IRF3-CBP-DNA interactions. Further, when cFLIPL was knocked down in various tumor cell lines, levels of tumor protective interferon stimulated genes (ISGs) increased, suggesting cFLIPL may contribute to tumorigenesis by way of inhibiting IRF3. In addition, cFLIPL also inhibited IFNa production by inhibiting the transcription factor, IRF7. In this case, the CLD of cFLIPL was dispensable to inhibit IFNa production; an alternative shorter isoform, cFLIPS, which lacks the CLD, also inhibited IRF7-induced IFNa expression. IRF7 phosphorylation was greatly reduced in cells expressing cFLIPL and cFLIPS. I hypothesized cFLIP targeted the IKK kinase. In support of this hypothesis, I found that cFLIPL co-IPs with IKa and IKKa-IRF7 interactions were disrupted in the presence of cFLIPL. These interactions were confirmed in a pDC-like cell line overexpressing cFLIP, suggesting that the mechanism by which cFLIP inhibits IFN production is physiologically relevant. Taken together, these data suggest that cFLIP is a major regulator of type I IFNs. It is of major clinical interest to regard the regulation of type I IFN expression by cFLIP when considering the pathophysiology behind diseases like cancer and autoimmunity. Advisors/Committee Members: Shisler, Joanna (advisor), Shisler, Joanna (Committee Chair), Blanke, Steven (committee member), Vanderpool, Cari (committee member), Wilson, Brenda (committee member).

Subjects/Keywords: cFLIP; interferon, innate; immunity

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Gates-Tanzer, L. T. (2018). Characterization of the anti-type I interferon effects of the cellular flice-like inhibitory protein (CFLIP). (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/101696

Chicago Manual of Style (16^th Edition):

Gates-Tanzer, Lauren Taylor. “Characterization of the anti-type I interferon effects of the cellular flice-like inhibitory protein (CFLIP).” 2018. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed January 23, 2021. http://hdl.handle.net/2142/101696.

MLA Handbook (7^th Edition):

Gates-Tanzer, Lauren Taylor. “Characterization of the anti-type I interferon effects of the cellular flice-like inhibitory protein (CFLIP).” 2018. Web. 23 Jan 2021.

Vancouver:

Gates-Tanzer LT. Characterization of the anti-type I interferon effects of the cellular flice-like inhibitory protein (CFLIP). [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2018. [cited 2021 Jan 23]. Available from: http://hdl.handle.net/2142/101696.

Council of Science Editors:

Gates-Tanzer LT. Characterization of the anti-type I interferon effects of the cellular flice-like inhibitory protein (CFLIP). [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2018. Available from: http://hdl.handle.net/2142/101696

University of Ottawa

21. Sam, Leila. Impact of Parkinson’s Disease- Linked- Lrrk2 Mutation (Lrrk2G2019S) on the Innate Immune Response During Infection with Listeria Monocytogenes.

Degree: MSc, Médecine / Medicine, 2020, University of Ottawa

URL: http://dx.doi.org/10.20381/ruor-25414

► Mutations in the Leucine-rich repeat kinase 2 (Lrrk2) gene are associated with familial and sporadic cases of Parkinson’s disease but are also found in inflammatory-related… (more)

▼ Mutations in the Leucine-rich repeat kinase 2 (Lrrk2) gene are associated with familial and sporadic cases of Parkinson’s disease but are also found in inflammatory-related disorders such as Crohn’s disease, systemic lupus erythematosus, tuberculosis and leprosy. There is also evidence that LRRK2 is highly expressed in immune cells, particularly in macrophages, and has been functionally linked to pathways pertinent to immune cell function such as modulating the course of infections, cytokine release, autophagy and phagocytosis. Indeed, G2019S mutation in Lrrk2 is the most common mutation in Parkinson’s disease. Accordingly, we hypothesized that G2019S mutation in Lrrk2 might enhance the activation of the innate immune system. We tested our hypothesis by performing challenge experiments in a mouse model of Listeria monocytogenes, and by measuring the activation of bone marrow derived macrophages (BMDMs) following in vitro infection with the bacterium. We found that Lrrk2G2019S mutant mice controlled L. monocytogenes better than WT mice. The mechanism behind the better control of L. monocytogenes by the G2019S mutation of Lrrk2 was investigated in BMDMs following in vitro infection with L. monocytogenes. Interestingly, we found that Lrrk2G2019S mutation enhances the production of TNF-α, IL-1β and IL-10 by infected BMDMs. The impact on TNF-α and IL-1β was specifically due to the G2019S mutation of Lrrk2 since there was no impact on the expression of these cytokines in Lrrk2 knockout macrophages. Western blotting experiments revealed that the G2019S mutation of Lrrk2 enhances MAPK signaling (TAK1, p38 and ERK). Modulation of the expression of the pro-inflammatory cytokines, TNF-α and IL-1β by G2019S mutation of Lrrk2 occurred via p38 MAPK activation. The impact on IL-10 expression occurred through increased ERK activation by the G2019S mutation of Lrrk2. We did not observe any impact of G2019S mutation of Lrrk2 on the activation of NF-κB and JNK MAPK pathways. Increased expression of IL-1β by G2019S mutation of Lrrk2 revealed increased inflammasome signaling. Inflammasome signaling in response to L. monocytogenes was mainly mediated by the AIM2- and partly by NLRP3- inflammasome and was dependent on activation of caspase-1. We found that Lrrk2G2019S mutation enhanced the expression of NLRP3 and caspase-1. Finally, we found that the expression of reactive oxygen species (ROS) following infection with L. monocytogenes was augmented by G2019S mutation of Lrrk2, and this can be an important mechanism that promotes the enhanced clearance of the bacterium in vivo. Overall, these results present new insights into the signaling mechanisms through which the G2019S mutation of Lrrk2 augments innate immune response which leads to better control of infection. Advisors/Committee Members: Sad, Subash (supervisor).

Subjects/Keywords: Lrrk2; Listeria monocytogenes; innate immunity

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sam, L. (2020). Impact of Parkinson’s Disease- Linked- Lrrk2 Mutation (Lrrk2G2019S) on the Innate Immune Response During Infection with Listeria Monocytogenes. (Masters Thesis). University of Ottawa. Retrieved from http://dx.doi.org/10.20381/ruor-25414

Chicago Manual of Style (16^th Edition):

Sam, Leila. “Impact of Parkinson’s Disease- Linked- Lrrk2 Mutation (Lrrk2G2019S) on the Innate Immune Response During Infection with Listeria Monocytogenes.” 2020. Masters Thesis, University of Ottawa. Accessed January 23, 2021. http://dx.doi.org/10.20381/ruor-25414.

MLA Handbook (7^th Edition):

Sam, Leila. “Impact of Parkinson’s Disease- Linked- Lrrk2 Mutation (Lrrk2G2019S) on the Innate Immune Response During Infection with Listeria Monocytogenes.” 2020. Web. 23 Jan 2021.

Vancouver:

Sam L. Impact of Parkinson’s Disease- Linked- Lrrk2 Mutation (Lrrk2G2019S) on the Innate Immune Response During Infection with Listeria Monocytogenes. [Internet] [Masters thesis]. University of Ottawa; 2020. [cited 2021 Jan 23]. Available from: http://dx.doi.org/10.20381/ruor-25414.

Council of Science Editors:

Sam L. Impact of Parkinson’s Disease- Linked- Lrrk2 Mutation (Lrrk2G2019S) on the Innate Immune Response During Infection with Listeria Monocytogenes. [Masters Thesis]. University of Ottawa; 2020. Available from: http://dx.doi.org/10.20381/ruor-25414

University of Cambridge

22. Digby, Zsofia. Caspase isoforms in inflammasome activation.

Degree: PhD, 2020, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/307833

► Inflammasomes are macromolecular signalling platforms composed of a receptor (for example NLRP3 or NLRC4), an adaptor (ASC) and effectors (caspases) that are thought to play… (more)

▼ Inflammasomes are macromolecular signalling platforms composed of a receptor (for example NLRP3 or NLRC4), an adaptor (ASC) and effectors (caspases) that are thought to play critical roles in the host defence against microbial infections. Activation of inflammasomes leads to the processing of the pro-inflammatory cytokines pro-IL-1β and pro- IL-18 to their active form and cleavage of gasdermin D to induce pyroptosis. Caspase-1 is the main inflammatory caspase responsible for cytokine maturation and induction of cell death, while human caspase-4, -5 and the mouse orthologue caspase-11 play an essential role in cytosolic bacterial LPS recognition. The putative importance of inflammasomes suggest that their constituents should be conserved across different animal species, but there are major differences, particularly in the caspase repertoire, in both invertebrates and vertebrates. The dog (Canis lupus familiaris), for example, has a pseudogene for NLRC4 and has a unique caspase-1/4/11 hybrid gene (CASP1-4/5/11) comprising the caspase-1 caspase recruitment domain (CARD) and the catalytic domain of caspase-4/5/11. Dogs produce bioactive IL-1β despite the apparent lack of the catalytically active domain of caspase-1, but how this occurs and whether inflammasome activation of CASP1-4/5/11 is required remains to be resolved. In this study I characterised inflammasome function in dog macrophages (DH82 cell line) and mouse macrophages where a caspase 1/4/11 fusion protein that is functional equivalent to CASP1-4/5/11 (DogMo) had been generated by CRISPR/Cas9 gene editing. I used imaging (ASC and active caspase speck formation), cell death analysis and IL-β production as readouts before and after editing of key genes in inflammasome formation using CRISPR-Cas9 gene editing approaches. The NLRP3 inflammasome is functional in dog macrophages, but the rate of inflammasome formation is lower compared to wild-type murine macrophages. This suggests that dog macrophages may be adapted to be tolerant to NLRP3 inflammasome activation only undergoing lytic cell death and IL-1β maturation when exposed to high concentrations of NLRP3 inflammasome activating ligands. DogMo cells retained full NLRP3 functionality. Cytosolic LPS-induced non-canonical inflammasome activation induced IL-1β maturation and secretion without concomitant cell death induction in dog macrophages. No ASC speck formation or activated caspase speck was seen suggesting there are alternative pathways for cytosolic LPS recognition and the consequential IL-1β maturation. DogMo cells did not induce non-canonical inflammasome formation. The NLRC4 inflammasome should not function in the dog and indeed DH82 cells infected with wild-type S. Typhimurium showed no ASC speck formation or active caspase recruitment and delayed cell death (compared to their wild-type mouse counterpart), but cleaved IL-1β was present in the supernatant. The processed IL-1β was smaller than the p17 fragment normally associated with cleavage by caspase-1. DogMo cells, which express NLRC4, did not…

Subjects/Keywords: immunology; innate immunity; inflammasome

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Digby, Z. (2020). Caspase isoforms in inflammasome activation. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/307833

Chicago Manual of Style (16^th Edition):

Digby, Zsofia. “Caspase isoforms in inflammasome activation.” 2020. Doctoral Dissertation, University of Cambridge. Accessed January 23, 2021. https://www.repository.cam.ac.uk/handle/1810/307833.

MLA Handbook (7^th Edition):

Digby, Zsofia. “Caspase isoforms in inflammasome activation.” 2020. Web. 23 Jan 2021.

Vancouver:

Digby Z. Caspase isoforms in inflammasome activation. [Internet] [Doctoral dissertation]. University of Cambridge; 2020. [cited 2021 Jan 23]. Available from: https://www.repository.cam.ac.uk/handle/1810/307833.

Council of Science Editors:

Digby Z. Caspase isoforms in inflammasome activation. [Doctoral Dissertation]. University of Cambridge; 2020. Available from: https://www.repository.cam.ac.uk/handle/1810/307833

University of Illinois – Urbana-Champaign

23. Granger, Kyle L. A pilot study on the effects of sow management practices on piglet immune responsiveness to weaning stress.

Degree: MS, Animal Sciences, 2016, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/95266

► The consequences of maternal prenatal stress exposure of the gestating sow on the developing immune system of her offspring is not well understood. There is… (more)

▼ The consequences of maternal prenatal stress exposure of the gestating sow on the developing immune system of her offspring is not well understood. There is limited data that primarily focuses on the health and well-being of the neonates of livestock animals, principally within the swine industry, in relation to the presence of unavoidable production stressors, including—but not limited to—weaning, mixing and social hierarchy. Each of the aforementioned stressors has been previously shown to affect the health, well-being, performance and productivity of sows as well as exacerbate the disease process by compromising the immune system. Thus, more information is needed to elucidate the complex relationship between prenatal stressors and postnatal immunological competence of the offspring. The objective of this thesis was to assess the effects of sow housing environment, social stress, and dietary fiber treatments during gestation on the immune and stress responsiveness of their progeny to weaning stress. Piglets were obtained from a larger-scale study of a 180 group-housed gestating sows. Briefly, sows were randomly allotted to 1 of 2 high fiber gestation diets (1) 30% wheat middlings and 15% soybean hulls (MID-SOY) or 30% distillers dried grains and 30% corn germ meal (DDG-GM) and to a group pen with feeding stalls of either 0.6 m (SHT) or 1.8 m (LNG) in length. Sows were fed dietary treatments starting on gestational d 35 and then moved to treatment pens at gestational d 37 and kept until d 104. On d 37, prior to moving into their experimental pens, a subsample of sows were subjected to a dominance test by which we determined a dominance value (DV). Those sows with a high DV were labeled dominant (DOM) and those with a low DV were labeled submissive (SUB). From both the larger study and the subsample of sows, 40-42 piglets were selected (balanced across treatments) based on body weight prior to weaning, with the two heaviest and two lightest piglets from each litter being used. All piglets were weaned at 19 ± 2 d-of-age. Blood samples were taken 24h prior to weaning, and then 7 and 14 days post-weaning to assess descriptive and functional aspects of both innate and adaptive immunity and cortisol. These data revealed that piglets weaned from sows fed MID-SOY during gestation had a profile indicative of a skewed TH1 (cell-mediated) response, while piglets weaned from sows fed DDG-GM diet were skewed toward TH2 (humoral) response. Piglets from sows housed in pens with LNG feeding stalls were better able to cope with weaning stress compared to those piglets from sows housed in pens with SHT. Moreover, sow social status differentially impact piglet immune responsiveness to weaning stress. Piglets weaned from SUB sows had a greater cell-mediated immune response which may have cost them in terms of performance because piglets from DOM sows had improved performance. These results show that: (1) feeding gestating sows high fiber diets can impact the development and growth of her offspring; (2) physical environment of gestating… Advisors/Committee Members: Salak-Johnson, Janeen L (advisor), Gaskins, Rex (committee member), Dailey, Megan J (committee member).

Subjects/Keywords: adaptive immunity; gestation; innate immunity; piglet; weaning

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Granger, K. L. (2016). A pilot study on the effects of sow management practices on piglet immune responsiveness to weaning stress. (Thesis). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/95266

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Granger, Kyle L. “A pilot study on the effects of sow management practices on piglet immune responsiveness to weaning stress.” 2016. Thesis, University of Illinois – Urbana-Champaign. Accessed January 23, 2021. http://hdl.handle.net/2142/95266.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Granger, Kyle L. “A pilot study on the effects of sow management practices on piglet immune responsiveness to weaning stress.” 2016. Web. 23 Jan 2021.

Vancouver:

Granger KL. A pilot study on the effects of sow management practices on piglet immune responsiveness to weaning stress. [Internet] [Thesis]. University of Illinois – Urbana-Champaign; 2016. [cited 2021 Jan 23]. Available from: http://hdl.handle.net/2142/95266.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Granger KL. A pilot study on the effects of sow management practices on piglet immune responsiveness to weaning stress. [Thesis]. University of Illinois – Urbana-Champaign; 2016. Available from: http://hdl.handle.net/2142/95266

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Dalhousie University

24. Moore, Jill Alexandra. Implications of the Innate Immune Response in Tuberculosis and Cardiac Allograft Vasculopathy.

Degree: MS, Department of Pathology, 2014, Dalhousie University

URL: http://hdl.handle.net/10222/53157

► Reactivation of latent tuberculosis (TB) in HIV-infected individuals has arisen as a major contributor to early death in areas where TB and HIV overlap. CD4+… (more)

Subjects/Keywords: innate immunity, macrophages, tuberculosis; innate immunity, macrophages, atherosclerosis, cardiac transplantation

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Moore, J. A. (2014). Implications of the Innate Immune Response in Tuberculosis and Cardiac Allograft Vasculopathy. (Masters Thesis). Dalhousie University. Retrieved from http://hdl.handle.net/10222/53157

Chicago Manual of Style (16^th Edition):

Moore, Jill Alexandra. “Implications of the Innate Immune Response in Tuberculosis and Cardiac Allograft Vasculopathy.” 2014. Masters Thesis, Dalhousie University. Accessed January 23, 2021. http://hdl.handle.net/10222/53157.

MLA Handbook (7^th Edition):

Moore, Jill Alexandra. “Implications of the Innate Immune Response in Tuberculosis and Cardiac Allograft Vasculopathy.” 2014. Web. 23 Jan 2021.

Vancouver:

Moore JA. Implications of the Innate Immune Response in Tuberculosis and Cardiac Allograft Vasculopathy. [Internet] [Masters thesis]. Dalhousie University; 2014. [cited 2021 Jan 23]. Available from: http://hdl.handle.net/10222/53157.

Council of Science Editors:

Moore JA. Implications of the Innate Immune Response in Tuberculosis and Cardiac Allograft Vasculopathy. [Masters Thesis]. Dalhousie University; 2014. Available from: http://hdl.handle.net/10222/53157

Colorado State University

25. Bickett, Thomas. T cell independent mechanisms for protection against Mycobacterium tuberculosis infection.

Degree: PhD, Cell and Molecular Biology, 2019, Colorado State University

URL: http://hdl.handle.net/10217/197402

► The live attenuated Mycobacterium bovis strain Bacille Calmette Guérin (BCG) is a potent innate immune stimulator. Innate Immunity provides the host with the ability to… (more)

Subjects/Keywords: innate immunity; trained innate immunity; tuberculosis; macrophage; BCG

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Bickett, T. (2019). T cell independent mechanisms for protection against Mycobacterium tuberculosis infection. (Doctoral Dissertation). Colorado State University. Retrieved from http://hdl.handle.net/10217/197402

Chicago Manual of Style (16^th Edition):

Bickett, Thomas. “T cell independent mechanisms for protection against Mycobacterium tuberculosis infection.” 2019. Doctoral Dissertation, Colorado State University. Accessed January 23, 2021. http://hdl.handle.net/10217/197402.

MLA Handbook (7^th Edition):

Bickett, Thomas. “T cell independent mechanisms for protection against Mycobacterium tuberculosis infection.” 2019. Web. 23 Jan 2021.

Vancouver:

Bickett T. T cell independent mechanisms for protection against Mycobacterium tuberculosis infection. [Internet] [Doctoral dissertation]. Colorado State University; 2019. [cited 2021 Jan 23]. Available from: http://hdl.handle.net/10217/197402.

Council of Science Editors:

Bickett T. T cell independent mechanisms for protection against Mycobacterium tuberculosis infection. [Doctoral Dissertation]. Colorado State University; 2019. Available from: http://hdl.handle.net/10217/197402

26. Schrum, Jacob E. Pathways Involved in Recognition and Induction of Trained Innate Immunity by Plasmodium falciparum.

Degree: PhD, Department of Medicine, Division of Infectious Diseases and Immunology, 2017, U of Massachusetts : Med

URL: http://escholarship.umassmed.edu/gsbs_diss/917

► Malarial infection in naïve individuals induces a robust innate immune response, but our understanding of the mechanisms by which the innate immune system recognizes… (more)

Subjects/Keywords: Plasmodium falciparum; innate immunity; innate immune memory; cGAS; trained immunity; Immunity; Immunology of Infectious Disease

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Schrum, J. E. (2017). Pathways Involved in Recognition and Induction of Trained Innate Immunity by Plasmodium falciparum. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from http://escholarship.umassmed.edu/gsbs_diss/917

Chicago Manual of Style (16^th Edition):

Schrum, Jacob E. “Pathways Involved in Recognition and Induction of Trained Innate Immunity by Plasmodium falciparum.” 2017. Doctoral Dissertation, U of Massachusetts : Med. Accessed January 23, 2021. http://escholarship.umassmed.edu/gsbs_diss/917.

MLA Handbook (7^th Edition):

Schrum, Jacob E. “Pathways Involved in Recognition and Induction of Trained Innate Immunity by Plasmodium falciparum.” 2017. Web. 23 Jan 2021.

Vancouver:

Schrum JE. Pathways Involved in Recognition and Induction of Trained Innate Immunity by Plasmodium falciparum. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2017. [cited 2021 Jan 23]. Available from: http://escholarship.umassmed.edu/gsbs_diss/917.

Council of Science Editors:

Schrum JE. Pathways Involved in Recognition and Induction of Trained Innate Immunity by Plasmodium falciparum. [Doctoral Dissertation]. U of Massachusetts : Med; 2017. Available from: http://escholarship.umassmed.edu/gsbs_diss/917

27. Evans, John W., III. Itk is a Dual Action Regulator of Immunoreceptor Signaling in the Innate and Adaptive Immune System: A Dissertation.

Degree: Immunology and Microbiology, Pathology, 2013, U of Massachusetts : Med

URL: http://escholarship.umassmed.edu/gsbs_diss/688

► The cells and molecules that comprise the immune system are essential for mounting an effective response against microbes. A successful immune response limits pathology… (more)

▼ The cells and molecules that comprise the immune system are essential for mounting an effective response against microbes. A successful immune response limits pathology within the host while simultaneously eliminating the pathogen. The key to this delicate balance is the correct recognition of the pathogen and the appropriate response of immune cells. Cellular activation originates through receptors that relay information about the state of the microenvironment to different compartments within the cell. The rapid relay of information is called signal transduction and employs a network of signaling mediators such as kinases, phosphatases, adaptor molecules, and transcription factors. IL-2 inducible T cell kinase (Itk) is a non-receptor tyrosine kinase that is an integral component of signal transduction downstream of many immunoreceptors. This dissertation describes two distinct pathways that utilize Itk in both phases of the immune response. T cells use the TCR to sense a multitude of peptide-based ligands and to transmit signals inside the cell to activate cellular function. In this regard, the diversity of ligands the T cells encounter can be portrayed as analog inputs. Once a critical threshold is met, signaling events transpire in close proximity to the plasma membrane to activate major downstream pathways in the cell. The majority of these pathways are digital in nature resulting in the on or off activation of T cells. We find, however, that altering the TCR signal strength that a T cell receives can result in an analog-based response. Here, the graded expression of a transcription factor, IRF4, is modulated through the activity of Itk. We link this graded response to an NFAT-mediated pathway in which the digital vs. analog nature has been previously uncharacterized. Finally, we demonstrate that the repercussions of an analog signaling pathway is the altered expression of a second transcription factor, Eomes, which is important in the differentiation and function of T cells. These results suggest that Itk is crucial in the modulation of TCR signal strength. Mast cells primarily rely on the IgE-bound FcεR1 for pathogen recognition. Crosslinking this receptor activates mast cells and results in degranulation and cytokine production via an expansive signaling cascade. Upon stimulation, Itk is recruited to the plasma membrane and phosphorylated. Little else is known about how Itk operates inside of mast cells. We find that mast cells lacking Itk are hyperresponsive to FcεR1-mediated activation. This is most apparent in the amount of IL-4 and IL-13 produced in comparison to wild-type mast cells. Increased cytokine production was accompanied by elevated and sustained signaling downstream of the FcεR1. Finally, biochemical evidence demonstrates that Itk is part of an inhibitory complex containing the phosphatase SHIP-1. These results indicate a novel function for Itk as a negative regulator in FcεR1- mediated mast cell activation. Advisors/Committee Members: Leslie J. Berg, PhD.

Subjects/Keywords: Signal Transduction; Protein-Tyrosine Kinases; Adaptive Immunity; Innate Immunity; Immunity; Immunopathology

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Evans, John W., I. (2013). Itk is a Dual Action Regulator of Immunoreceptor Signaling in the Innate and Adaptive Immune System: A Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from http://escholarship.umassmed.edu/gsbs_diss/688

Chicago Manual of Style (16^th Edition):

Evans, John W., III. “Itk is a Dual Action Regulator of Immunoreceptor Signaling in the Innate and Adaptive Immune System: A Dissertation.” 2013. Doctoral Dissertation, U of Massachusetts : Med. Accessed January 23, 2021. http://escholarship.umassmed.edu/gsbs_diss/688.

MLA Handbook (7^th Edition):

Evans, John W., III. “Itk is a Dual Action Regulator of Immunoreceptor Signaling in the Innate and Adaptive Immune System: A Dissertation.” 2013. Web. 23 Jan 2021.

Vancouver:

Evans, John W. I. Itk is a Dual Action Regulator of Immunoreceptor Signaling in the Innate and Adaptive Immune System: A Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2013. [cited 2021 Jan 23]. Available from: http://escholarship.umassmed.edu/gsbs_diss/688.

Council of Science Editors:

Evans, John W. I. Itk is a Dual Action Regulator of Immunoreceptor Signaling in the Innate and Adaptive Immune System: A Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 2013. Available from: http://escholarship.umassmed.edu/gsbs_diss/688

28. Ho, Eric Chun Hei. A Simple Animal Model for Characterizing Gene Reglatory Control of an Immune Response.

Degree: PhD, 2016, University of Toronto

URL: http://hdl.handle.net/1807/73011

► A robust but tightly regulated system of innate gut immunity is required for maintaining gut homeostasis. Given the complex nature of the mammalian gut, a… (more)

▼ A robust but tightly regulated system of innate gut immunity is required for maintaining gut homeostasis. Given the complex nature of the mammalian gut, a simple yet phylogenetically relevant model is useful to decipher the underlying molecular controls that sustain this balance. Here I use the purple sea urchin larva as a morphologically simple model for these studies. I approach this problem with three interrelated strategies: (1) Characterization of larval immunocytes based on morphology, cell behaviour and gene expression, (2) analysis of gene activity in a model of gut-associated immune response to bacteria and (3) regulatory analysis of selected response genes. I characterize five larval cell types that are active in gut immunity and develop a gut associated infection model using the bacterium Vibrio diazotrophicus. RNA-seq analysis of this model is used to identify immune genes that are differentially expressed over the course of infection. Member of the sea urchin IL-17 multigene family are identified as immune response genes. One subfamily, SpIL-17-I, is expressed early upon exposure to V. diazotrophicus in the mid- and hindgut and is then attenuated. BAC-based GFP transgenes and smaller reporter constructs recapitulate endogenous SpIL-17-I expression. Regulatory regions are defined upstream and downstream of the IL-17 coding sequence. Deletions of critical elements results in a decrease or absence of IL-17 expression but never ectopic expression or expression in the absence of immune stimulus. Downstream function of IL-17 was investigated by perturbing its receptors using Morpholino antisense oligonucleotides. In addition to physiological changes in the larva, expression of several immune effector genes are downregulated in IL-17R perturbed embryos. Collectively this work suggests that a core network of regulatory circuitry is shared with the vertebrates in the gut associated immune response even in this simple larval form. This can then form the basis for more elaborate network analysis of gut immunity in future studies using this model. Advisors/Committee Members: Rast, Jonathan P, Medical Biophysics.

Subjects/Keywords: comparative immunity; gut immunity; IL-17; innate immunity; sea urchin; 0982

12 more images…

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ho, E. C. H. (2016). A Simple Animal Model for Characterizing Gene Reglatory Control of an Immune Response. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/73011

Chicago Manual of Style (16^th Edition):

Ho, Eric Chun Hei. “A Simple Animal Model for Characterizing Gene Reglatory Control of an Immune Response.” 2016. Doctoral Dissertation, University of Toronto. Accessed January 23, 2021. http://hdl.handle.net/1807/73011.

MLA Handbook (7^th Edition):

Ho, Eric Chun Hei. “A Simple Animal Model for Characterizing Gene Reglatory Control of an Immune Response.” 2016. Web. 23 Jan 2021.

Vancouver:

Ho ECH. A Simple Animal Model for Characterizing Gene Reglatory Control of an Immune Response. [Internet] [Doctoral dissertation]. University of Toronto; 2016. [cited 2021 Jan 23]. Available from: http://hdl.handle.net/1807/73011.

Council of Science Editors:

Ho ECH. A Simple Animal Model for Characterizing Gene Reglatory Control of an Immune Response. [Doctoral Dissertation]. University of Toronto; 2016. Available from: http://hdl.handle.net/1807/73011

Universiteit Utrecht

29. Fermie, J. Failure of Immunity Against Hepatitis C Virus: Implications of Defects in Early Immunity.

Degree: 2013, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/283340

► The hepatitis C virus (HCV) is an upcoming human pathogen. Although HCV infection is mostly asymptomatic, persistent infection may lead to liver failure or liver… (more)

Subjects/Keywords: HCV; Hepatitis C Virus; Adaptive immunity; Innate immunity; T cell; chronic infection; viral immunity; immunity

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Fermie, J. (2013). Failure of Immunity Against Hepatitis C Virus: Implications of Defects in Early Immunity. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/283340

Chicago Manual of Style (16^th Edition):

Fermie, J. “Failure of Immunity Against Hepatitis C Virus: Implications of Defects in Early Immunity.” 2013. Masters Thesis, Universiteit Utrecht. Accessed January 23, 2021. http://dspace.library.uu.nl:8080/handle/1874/283340.

MLA Handbook (7^th Edition):

Fermie, J. “Failure of Immunity Against Hepatitis C Virus: Implications of Defects in Early Immunity.” 2013. Web. 23 Jan 2021.

Vancouver:

Fermie J. Failure of Immunity Against Hepatitis C Virus: Implications of Defects in Early Immunity. [Internet] [Masters thesis]. Universiteit Utrecht; 2013. [cited 2021 Jan 23]. Available from: http://dspace.library.uu.nl:8080/handle/1874/283340.

Council of Science Editors:

Fermie J. Failure of Immunity Against Hepatitis C Virus: Implications of Defects in Early Immunity. [Masters Thesis]. Universiteit Utrecht; 2013. Available from: http://dspace.library.uu.nl:8080/handle/1874/283340

NSYSU

30. Chang, Jenn-tzong. Genome and Infection Characteristics of Human Parechovirus Type 1.

Degree: PhD, Biological Sciences, 2015, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0521115-005317

► Human parechoviruses (HPeVs), members of the family Picornaviridae, are associated with severe human clinical conditions such as gastrointestinal disease, encephalitis, meningitis, respiratory disease and neonatal… (more)

Subjects/Keywords: type I interferon; parechovirus; HPeV; innate immunity

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Chang, J. (2015). Genome and Infection Characteristics of Human Parechovirus Type 1. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0521115-005317

Chicago Manual of Style (16^th Edition):

Chang, Jenn-tzong. “Genome and Infection Characteristics of Human Parechovirus Type 1.” 2015. Doctoral Dissertation, NSYSU. Accessed January 23, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0521115-005317.

MLA Handbook (7^th Edition):

Chang, Jenn-tzong. “Genome and Infection Characteristics of Human Parechovirus Type 1.” 2015. Web. 23 Jan 2021.

Vancouver:

Chang J. Genome and Infection Characteristics of Human Parechovirus Type 1. [Internet] [Doctoral dissertation]. NSYSU; 2015. [cited 2021 Jan 23]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0521115-005317.

Council of Science Editors:

Chang J. Genome and Infection Characteristics of Human Parechovirus Type 1. [Doctoral Dissertation]. NSYSU; 2015. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0521115-005317

		in
And / Or
		in
And / Or
		in
And / Or
		in

Open Access Theses and Dissertations