subject:(Dendritic cell migration)

Penn State University

1. Fischer, Matthew Anthony. The Immune Response to Vaccinia Virus Infection: Inflammatory Monocytes, Leukotrienes, and CD8+ T Cell Immunodominance.

Degree: PhD, Microbiology and Immunology, 2009, Penn State University

URL: https://etda.libraries.psu.edu/catalog/10147

► Although Vaccinia virus (VACV) has been used extensively as a vaccine to convey protection against other poxviruses and, through the expression of recombinant antigens, other… (more)

▼ Although Vaccinia virus (VACV) has been used extensively as a vaccine to convey protection against other poxviruses and, through the expression of recombinant antigens, other pathogens and tumors, several problems exist that limit its potential use within the human population. Two such problems are the dangerous complications of uncontrolled viral replication and the immunodominance of VACV-specific CD8+ T cells. The immune mechanisms responsible for controlling VACV replication at the site of infection were previously unclear. Although adaptive immunity is often given credit for this function, viral titers begin to lower during the innate immune response. Through in vivo cellular depletions, we demonstrated that inflammatory monocytes, including a Ly6C+Ly6G+ subpopulation, are critical factors for controlling VACV replication at the site of infection, preventing spread of the virus to other sites, and limiting immune-mediated tissue damage. Leukotrienes are potent mediators of the innate immune response capable of affecting the monocytic response, although their precise functions in the skin and in viral infections are poorly understood. In MRP1 knockout mice, we observed exacerbated inflammation and tissue damage during an intradermal VACV infection. These effects were not due to a lack of cysteinyl leukotrienes as the use of a cysteinyl leukotriene receptor antagonist alleviated tissue damage. Rather, increased leukotriene B4 levels in MRP1 knockout mice were responsible. When recombinant VACV constructs are utilized to induce CD8+ T cells specific for a recombinantly encoded foreign antigen, the majority of the CD8+ T cell response is directed against VACV. We utilized UV and psoralen treatment to globally reduce the expression of native VACV genes while relatively maintaining the expression of a recombinant antigenic peptide. This increased the primary CD8+ T cell response specific for the recombinant antigen, while decreasing VACV-specific CD8+ T cells. Our findings have implications for the safe and effective use of VACV as a human vaccine. By therapeutically targeting monocytes and/or leukotrienes, the innate immune response can be manipulated to improve the safety of VACV immunization. Further, UV/psoralen treated recombinant VACV constructs represent more effective vaccine vectors for inducing antigen-specific CD8+ T cells.

Subjects/Keywords: immunodominance; leukotrienes; inflammatory monocytes; Vaccinia virus; dendritic cell migration

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

APA (6^th Edition):

Fischer, M. A. (2009). The Immune Response to Vaccinia Virus Infection: Inflammatory Monocytes, Leukotrienes, and CD8+ T Cell Immunodominance. (Doctoral Dissertation). Penn State University. Retrieved from https://etda.libraries.psu.edu/catalog/10147

Chicago Manual of Style (16^th Edition):

Fischer, Matthew Anthony. “The Immune Response to Vaccinia Virus Infection: Inflammatory Monocytes, Leukotrienes, and CD8+ T Cell Immunodominance.” 2009. Doctoral Dissertation, Penn State University. Accessed October 21, 2019. https://etda.libraries.psu.edu/catalog/10147.

MLA Handbook (7^th Edition):

Fischer, Matthew Anthony. “The Immune Response to Vaccinia Virus Infection: Inflammatory Monocytes, Leukotrienes, and CD8+ T Cell Immunodominance.” 2009. Web. 21 Oct 2019.

Vancouver:

Fischer MA. The Immune Response to Vaccinia Virus Infection: Inflammatory Monocytes, Leukotrienes, and CD8+ T Cell Immunodominance. [Internet] [Doctoral dissertation]. Penn State University; 2009. [cited 2019 Oct 21]. Available from: https://etda.libraries.psu.edu/catalog/10147.

Council of Science Editors:

Fischer MA. The Immune Response to Vaccinia Virus Infection: Inflammatory Monocytes, Leukotrienes, and CD8+ T Cell Immunodominance. [Doctoral Dissertation]. Penn State University; 2009. Available from: https://etda.libraries.psu.edu/catalog/10147

2. Batich, Kristen Anne. Enhancing Dendritic Cell Migration to Drive Antitumor Responses .

Degree: 2017, Duke University

URL: http://hdl.handle.net/10161/10453

► The histologic subtypes of malignant glial neoplasms range from anaplastic astrocytoma to the most deadly World Health Organization (WHO) Grade IV glioblastoma (GBM), the… (more)

▼ The histologic subtypes of malignant glial neoplasms range from anaplastic astrocytoma to the most deadly World Health Organization (WHO) Grade IV glioblastoma (GBM), the most common primary brain tumor in adults. Over the past 40 years, only modest advancements in the treatment of GBM tumors have been reached. Current therapies are predominantly for palliative endpoints rather than curative, although some treatment modalities have been shown to extend survival in particular cases. Patients undergoing current standard of care therapy, including surgical resection, radiation therapy, and chemotherapy, have a median survival of 12-15 months, with less than 25% of patients surviving up to two years and fewer than 10% surviving up to five years. A variety of factors contribute to standard treatment failure, including highly invasive tumor grade at the time of diagnosis, the intrinsic resistance of glioma cells to radiation therapy, the frequent impracticality of maximal tumor resection of eloquent cortical structures, and the fragile intolerance of healthy brain for cytotoxic therapies. Treatment with immunotherapy is a potential answer to the aforementioned problems, as the immune system can be harnessed and educated to license rather potent antitumor responses in a highly specific and safe fashion. One of the most promising vehicles for immunotherapy is the use of dendritic cells, which are professional antigen-presenting cells that are highly effective in the processing of foreign antigens and the education of soon-to-be activated T cells against established tumors. The work outlined in this dissertation encompasses the potential of dendritic cell therapy, the current limitations of reaching full efficacy with this platform, and the recent efforts employed to overcome such barriers. This work spans the characterization and preclinical testing of utilizing protein antigens such as tetanus-diphtheria toxoid to pre-condition the injection site prior to dendritic cell vaccination against established tumors expressing tumor-specific antigens. Chapter 1 comprises an overview of the current standard therapies for malignant brain tumors. Chapters 2 and 3 provide a review of immunotherapy for malignant gliomas in the setting of preclinical animal models and discuss issues relevant to the efficacy of dendritic cell vaccines for targeting of GBM. Chapters 4 provides the rationale, methodology, and results of research to improve the lymph node homing and immunogenicity of tumor antigen-specific dendritic cell vaccines in mouse models and in patients with newly diagnosed GBM. Chapter 5 delineates the interactions discovered through efforts in Chapter 4 that comprise protein antigen-specific CD4+ T cell responses to induced chemokines and how these interactions result in increased dendritic cell migration and antitumor responses. Lastly, Chapter 6 discusses the future utility of migration of DC vaccines as a surrogate for antitumor responses and clinical outcomes. This dissertation comprises original… Advisors/Committee Members: Sampson, John H (advisor).

Subjects/Keywords: Immunology; Biology; dendritic cell; glioblastoma; malignant glioma; migration; tumor immunology

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APA (6^th Edition):

Batich, K. A. (2017). Enhancing Dendritic Cell Migration to Drive Antitumor Responses . (Thesis). Duke University. Retrieved from http://hdl.handle.net/10161/10453

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):

Batich, Kristen Anne. “Enhancing Dendritic Cell Migration to Drive Antitumor Responses .” 2017. Thesis, Duke University. Accessed October 21, 2019. http://hdl.handle.net/10161/10453.

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

MLA Handbook (7^th Edition):

Batich, Kristen Anne. “Enhancing Dendritic Cell Migration to Drive Antitumor Responses .” 2017. Web. 21 Oct 2019.

Vancouver:

Batich KA. Enhancing Dendritic Cell Migration to Drive Antitumor Responses . [Internet] [Thesis]. Duke University; 2017. [cited 2019 Oct 21]. Available from: http://hdl.handle.net/10161/10453.

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

Council of Science Editors:

Batich KA. Enhancing Dendritic Cell Migration to Drive Antitumor Responses . [Thesis]. Duke University; 2017. Available from: http://hdl.handle.net/10161/10453

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

3. Evans, Joseph Corey. Regulation of Dendritic Spine Development and Cell Migration through Asef2-mediated Signaling.

Degree: PhD, Biological Sciences, 2014, Vanderbilt University

URL: http://etd.library.vanderbilt.edu/available/etd-07232014-132105/ ;

► Rho GTPases are molecular switches that mediate the formation of dendritic spines â actin-enriched protrusions that make excitatory synapses with nearby neurons. Once activated by… (more)

▼ Rho GTPases are molecular switches that mediate the formation of dendritic spines â actin-enriched protrusions that make excitatory synapses with nearby neurons. Once activated by guanine nucleotide exchange factors (GEFs), GTPases regulate actin dynamics within spines. The roles of several Rho GTPases are known in spines; the functions of many GEFs, however, are unclear. Here, we show that the Rac GEF Asef2 is important for the development of dendritic spines. Endogenous Asef2 localizes to spines, and spine and synapse density can be increased or decreased by expression or knockdown of Asef2, respectively. This effect is GEF activity-dependent, since mutation of Asef2âs GEF domain blocks spine formation. Also, knockdown of Rac blocks Asef2-mediated spine formation, suggesting that Asef2 activates Rac to promote spine development. Finally, the actin-binding protein spinophilin also regulates Asef2 function by targeting Asef2 to spines. In a related project, we investigated the regulation of Asef2 activity by identifying putative phosphorylation sites. Six phosphorylation sites were identified by mass spectrometry. Most of these sites cluster around the autoinhibitory region of Asef2, suggesting that they may regulate Asef2 activity. To test this, one of the residues â serine 106 â was mutated to alanine (S106A, non-phosphorylatable analogue) or to aspartic acid (S106E, phosphomimetic analogue), and the effect of these mutations on cell migration (another actin-dependent process) was assessed. The S106A mutant inhibited Asef2-mediated Rac activation, cell migration, and adhesion turnover (a component of cell migration), while the S106E mutant promoted Rac activation but did not influence cell migration compared to wild-type Asef2. These results suggest that phosphorylation is an important mechanism for regulating Asef2 activity and function. Advisors/Committee Members: Terry Page (chair), Donna Webb (committee member), Alissa Weaver (committee member), Douglas McMahon (committee member), Bruce Carter (committee member).

Subjects/Keywords: dendritic spine; Guanine nucleotide exchange factor; neuron; Rho GTPases; cell migration

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APA (6^th Edition):

Evans, J. C. (2014). Regulation of Dendritic Spine Development and Cell Migration through Asef2-mediated Signaling. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-07232014-132105/ ;

Chicago Manual of Style (16^th Edition):

Evans, Joseph Corey. “Regulation of Dendritic Spine Development and Cell Migration through Asef2-mediated Signaling.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed October 21, 2019. http://etd.library.vanderbilt.edu/available/etd-07232014-132105/ ;.

MLA Handbook (7^th Edition):

Evans, Joseph Corey. “Regulation of Dendritic Spine Development and Cell Migration through Asef2-mediated Signaling.” 2014. Web. 21 Oct 2019.

Vancouver:

Evans JC. Regulation of Dendritic Spine Development and Cell Migration through Asef2-mediated Signaling. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2019 Oct 21]. Available from: http://etd.library.vanderbilt.edu/available/etd-07232014-132105/ ;.

Council of Science Editors:

Evans JC. Regulation of Dendritic Spine Development and Cell Migration through Asef2-mediated Signaling. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://etd.library.vanderbilt.edu/available/etd-07232014-132105/ ;

University of Toronto

4. Rajkumar, Andrew. The Role of Interleukin-1 Beta in Mediating LPS-Induced Reverse Transendothelial Migration of Intimal Dendritic Cells.

Degree: 2018, University of Toronto

URL: http://hdl.handle.net/1807/91394

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Intimal dendritic-like cells (DCs) reside in regions of the aorta predisposed to atherosclerosis. LPS and interleukin-1 beta (IL-1β) injections into C57BL/6 mice result in decreased… (more)

Subjects/Keywords: Dendritic Cell; Interleukin-1 Beta; Intima; Lipopolysaccharide; Reverse Transendothelial Migration; 0982

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

APA (6^th Edition):

Rajkumar, A. (2018). The Role of Interleukin-1 Beta in Mediating LPS-Induced Reverse Transendothelial Migration of Intimal Dendritic Cells. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/91394

Chicago Manual of Style (16^th Edition):

Rajkumar, Andrew. “The Role of Interleukin-1 Beta in Mediating LPS-Induced Reverse Transendothelial Migration of Intimal Dendritic Cells.” 2018. Masters Thesis, University of Toronto. Accessed October 21, 2019. http://hdl.handle.net/1807/91394.

MLA Handbook (7^th Edition):

Rajkumar, Andrew. “The Role of Interleukin-1 Beta in Mediating LPS-Induced Reverse Transendothelial Migration of Intimal Dendritic Cells.” 2018. Web. 21 Oct 2019.

Vancouver:

Rajkumar A. The Role of Interleukin-1 Beta in Mediating LPS-Induced Reverse Transendothelial Migration of Intimal Dendritic Cells. [Internet] [Masters thesis]. University of Toronto; 2018. [cited 2019 Oct 21]. Available from: http://hdl.handle.net/1807/91394.

Council of Science Editors:

Rajkumar A. The Role of Interleukin-1 Beta in Mediating LPS-Induced Reverse Transendothelial Migration of Intimal Dendritic Cells. [Masters Thesis]. University of Toronto; 2018. Available from: http://hdl.handle.net/1807/91394

Université de Montréal

5. Raymond, Marianne. Rôle des cellules dendritiques SIRPα+ dans l’asthme expérimental .

Degree: 2011, Université de Montréal

URL: http://hdl.handle.net/1866/4719

► L’asthme est une maladie multifactorielle hétérogène qui engendre une inflammation pulmonaire associée à une variété de manifestations cliniques, dont des difficultés respiratoires graves. Globalement, l’asthme… (more)

▼ L’asthme est une maladie multifactorielle hétérogène qui engendre une inflammation pulmonaire associée à une variété de manifestations cliniques, dont des difficultés respiratoires graves. Globalement, l’asthme touche environ une personne sur 6 et présente actuellement un sérieux problème de santé publique. Bien que de nombreux traitements soient disponibles pour soulager les symptômes de la maladie, aucun traitement curatif n’est actuellement disponible. La compréhension des mécanismes qui régissent l’état inflammatoire au cours de la maladie est primordiale à la découverte de nouvelles cibles thérapeutiques efficaces. Les cellules dendritiques captent les allergènes dans les poumons et migrent vers les ganglions drainants pour les présenter aux cellules T et engendrer la réponse inflammatoire pathogénique chez les asthmatiques. Nous avons contribué à l’avancement des connaissances mécanistiques de l’asthme en identifiant chez la souris la sous-population de cellules dendritiques responsable de l’initiation et du maintien de la réponse inflammatoire locale et systémique associée à l’asthme. En effet, nous avons démontré que le SIRPα, récepteur extracellulaire impliqué dans la régulation de la réponse immune, est sélectivement exprimé à la surface des cellules dendritiques immunogéniques. L’interruption de la liaison entre le SIRPα et son ligand, le CD47, interfère avec la migration des cellules dendritiques SIRPα+ et renverse la réponse inflammatoire allergique. Ce mécanisme constitue une avenue thérapeutique prometteuse. D’ailleurs, les molécules de fusion CD47-Fc et SIRPα-Fc se sont avérées efficaces pour inhiber l’asthme allergique dans le modèle murin. Nous avons également démontré l’implication des cellules dendritiques SIRPα dans un modèle d’inflammation pulmonaire sévère. L’administration répétée de ces cellules, localement par la voie intra-trachéale et systémiquement par la voie intra-veineuse, mène au développement d’une réponse inflammatoire mixte, de type Th2-Th17, similaire à celle observée chez les patients atteints d’asthme sévère. La présence de cellules T exprimant à la fois l’IL-17, l’IL-4, l’IL-13 et le GATA3 a été mise en évidence pour la première fois in vitro et in vivo dans les poumons et les ganglions médiastinaux grâce à ce modèle. Nos expériences suggèrent que ces cellules Th2-Th17 exploitent la plasticité des cellules T et sont générées à partir de la conversion de cellules Th17 qui acquièrent un phénotype Th2, et non l’inverse. Ces résultats approfondissent la compréhension des mécanismes impliqués dans l’initiation et le maintien de l’asthme allergique et non allergique, en plus d’ouvrir la voie à l’élaboration d’un traitement spécifique pour les patients asthmatiques, particulièrement ceux pour qui aucun traitement efficace n’est actuellement disponible. Advisors/Committee Members: Sarfati, Marika (advisor).

Subjects/Keywords: Asthme; Inflammation pulmonaire; Cellules Dendritiques; CD47; Sirp; Th2; Th17; Migration; Asthma; Airway Inflammation; Dendritic Cell; CD47; Sirp; Th2; Th17; Migration

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

APA (6^th Edition):

Raymond, M. (2011). Rôle des cellules dendritiques SIRPα+ dans l’asthme expérimental . (Thesis). Université de Montréal. Retrieved from http://hdl.handle.net/1866/4719

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):

Raymond, Marianne. “Rôle des cellules dendritiques SIRPα+ dans l’asthme expérimental .” 2011. Thesis, Université de Montréal. Accessed October 21, 2019. http://hdl.handle.net/1866/4719.

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

MLA Handbook (7^th Edition):

Raymond, Marianne. “Rôle des cellules dendritiques SIRPα+ dans l’asthme expérimental .” 2011. Web. 21 Oct 2019.

Vancouver:

Raymond M. Rôle des cellules dendritiques SIRPα+ dans l’asthme expérimental . [Internet] [Thesis]. Université de Montréal; 2011. [cited 2019 Oct 21]. Available from: http://hdl.handle.net/1866/4719.

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

Council of Science Editors:

Raymond M. Rôle des cellules dendritiques SIRPα+ dans l’asthme expérimental . [Thesis]. Université de Montréal; 2011. Available from: http://hdl.handle.net/1866/4719

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

University of Cincinnati

6. Thacker, Robert I. Modulation of Human Dendritic Cell Activity by Adsorbed Fibrin(ogen).

Degree: PhD, Medicine : Pathobiology and Molecular Medicine, 2008, University of Cincinnati

URL: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1218553202

► Fibrinogen, a plasma protein central to clot formation, has long been considered to play a role in inflammation and immunity. Fibrin(ogen) interactions with various immune… (more)

▼ Fibrinogen, a plasma protein central to clot formation, has long been considered to play a role in inflammation and immunity. Fibrin(ogen) interactions with various immune cells have been heavily investigated; lacking is an understanding of the protein's influence on dendritic cell activity. Results from Chapter 2 demonstrate that fibrinogen initiates human dendritic cell production of inflammatory cytokines and chemokines. Adsorbed fibrin(ogen) has increased stimulatory capacity over fibrin(ogen) free in solution, indicating the bound protein, acting through the ß₂-integrins, is the active species. Adsorbed fibrin(ogen) also stimulates the focal accumulation of dendritic cells. This is likely due to ß₂-integrin-mediated chemotaxis of dendritic cells toward released chemokines and fibrin(ogen) degradation fragments. Because studies suggested adsorbed fibrinogen might be exploited to enhance vaccine adjuvanticity, fibrinogen-coated olive oil droplets were investigated as vaccine adjuvant. Results from Chapter 3 demonstrate the importance of surface in adjuvant activity, and the possible use of olive oil droplets as a safe and effective vaccine adjuvant. Having investigated the interactions between fibrinogen-coated particles and human dendritic cells, Chapter 4 describes the existence of a not yet recorded phenomenon: extracellular transport of cell-sized particles by dendritic cells. Results presented in that chapter not only demonstrate particles can be carried extracellularly by dendritic cells, but also that the process can be directed. Adsorbed fibrin(ogen) appears to enhance particle/dendritic cell interactions mediated through the ß₂-integrins. The influence of adsorbed fibrin(ogen) on dendritic cells provides new knowledge into the protein's involvement in initiating inflammatory and immune responses, knowledge that may be applied to the development of new therapeutics to treat and prevent disease. Advisors/Committee Members: Retzinger, Gregory (Committee Chair).

Subjects/Keywords: Immunology; Pathology; fibrinogen; surfaces; inflammation; CD18; vaccine adjuvants; oil emulsion; dendritic cell; extracellular translocation; cancer metastasis; dendritic cell migration; olive oil; integrins; cytokine; chemokines

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

APA (6^th Edition):

Thacker, R. I. (2008). Modulation of Human Dendritic Cell Activity by Adsorbed Fibrin(ogen). (Doctoral Dissertation). University of Cincinnati. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ucin1218553202

Chicago Manual of Style (16^th Edition):

Thacker, Robert I. “Modulation of Human Dendritic Cell Activity by Adsorbed Fibrin(ogen).” 2008. Doctoral Dissertation, University of Cincinnati. Accessed October 21, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1218553202.

MLA Handbook (7^th Edition):

Thacker, Robert I. “Modulation of Human Dendritic Cell Activity by Adsorbed Fibrin(ogen).” 2008. Web. 21 Oct 2019.

Vancouver:

Thacker RI. Modulation of Human Dendritic Cell Activity by Adsorbed Fibrin(ogen). [Internet] [Doctoral dissertation]. University of Cincinnati; 2008. [cited 2019 Oct 21]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1218553202.

Council of Science Editors:

Thacker RI. Modulation of Human Dendritic Cell Activity by Adsorbed Fibrin(ogen). [Doctoral Dissertation]. University of Cincinnati; 2008. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1218553202

7. Kimura, Telma Fátima Emídio. Análise da capacidade migratória de células dendríticas na cromoblastomicose experimental.

Degree: Mestrado, Análises Clínicas, 2012, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/9/9136/tde-01032013-092230/ ;

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A cromoblastomicose é uma micose subcutânea, com alto índice de morbidade, sendo Fonsecaea pedrosoi (F. pedrosoi) considerado o maior agente etiológico dessa micose, caracterizando uma… (more)

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A cromoblastomicose é uma micose subcutânea, com alto índice de morbidade, sendo Fonsecaea pedrosoi (F. pedrosoi) considerado o maior agente etiológico dessa micose, caracterizando uma doença crônica, geralmente confinada na pele e tecidos subcutâneos. Raramente os indivíduos apresentam cura dessa doença, pois as terapias contemporâneas mostram-se deficientes e poucos trabalhos relatam a relação parasito-hospedeiro. As células dendríticas (DCs) são especializadas na apresentação de antígenos para linfócitos T naive induzindo respostas imunes primárias. Diante disso, propomos estudar a capacidade migratória de DCs após infecção com conídios de F. pedrosoi, uma vez que o processo de migração dessas células está intimamente ligado com a sua função sobre as células T, levando ao desenvolvimento de uma resposta imune adaptativa protetora. O fenótipo de DCs foi avaliado através de células obtidas dos linfonodos poplíteos, inguinais e patas de camundongos BALB/c após 12, 24 e 72 horas de infecção com conídios do fungo. Células obtidas foram marcadas com anticorpos específicos e analisadas por citometria de fluxo. Após 24 e 72 horas de infecção verificamos uma diminuição significativa na porcentagem de DCs nas patas, e um aumento significativo dessas células nos linfonodos após 72 horas. A expressão de marcadores de superfície como CCR7 e moléculas co-estimulatórias, mostraram-se diminuídas nas células obtidas das patas. Como no processo de imunofenotipagem podemos analisar DCs vindas de diversos locais, para melhor avaliar a capacidade migratória das DCs, células das patas foram marcadas in vivo injetando-se subcutaneamente o corante CFSE juntamente com conídios do fungo. Verificamos que após 12 e 72 horas, as DCs das patas dos animais infectados, migraram para os linfonodos regionais. Assim constatamos que o fungo F. pedrosoi é capaz de induzir a migração de macrófagos e neutrófilos para o sítio de infecção em poucas horas, leva ao aumento de células B nos linfonodos após 12 e 72 horas de infecção, e também leva ao aumento de linfócitos T CD4+ tanto no local de infecção quanto nos linfonodos. Os resultados também comprovam que o fungo F. pedrosoi foi capaz de ativar as DCs, induzindo sua migração para os linfonodos regionais.

The chromoblastomycosis is a subcutaneous mycosis with a high morbidity rate, Fonsecaea pedrosoi (F. Pedrosoi) being the largest etiologic agent of this mycosis, featuring a chronic disease, usually confined to the skin and subcutaneous tissues. Rarely do people have cure for this disease, because the therapies shown to be deficient contemporary and few studies report the host-parasite relationship. Dendritic cells (DCs) are specialized in presenting antigens to naïve T lymphocytes inducing primary immune responses. Therefore, we propose to study the migratory capacity of DCs after infection with conidia of F. pedrosoi, since the migration of these cells is intimately linked to its function on T cells, leading to development of a protective adaptive immune response. The phenotype of DCs was…

Advisors/Committee Members: Almeida, Sandro Rogerio de.

Subjects/Keywords: Cell migration; Células dendríticas; Chromoblastomycosis (Medicine); Cromoblastomicose (Medicina); Dendritic cells; Immunology; Imunologia; Medical micology; Micologia médica; Migração celular

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

APA (6^th Edition):

Kimura, T. F. E. (2012). Análise da capacidade migratória de células dendríticas na cromoblastomicose experimental. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/9/9136/tde-01032013-092230/ ;

Chicago Manual of Style (16^th Edition):

Kimura, Telma Fátima Emídio. “Análise da capacidade migratória de células dendríticas na cromoblastomicose experimental.” 2012. Masters Thesis, University of São Paulo. Accessed October 21, 2019. http://www.teses.usp.br/teses/disponiveis/9/9136/tde-01032013-092230/ ;.

MLA Handbook (7^th Edition):

Kimura, Telma Fátima Emídio. “Análise da capacidade migratória de células dendríticas na cromoblastomicose experimental.” 2012. Web. 21 Oct 2019.

Vancouver:

Kimura TFE. Análise da capacidade migratória de células dendríticas na cromoblastomicose experimental. [Internet] [Masters thesis]. University of São Paulo; 2012. [cited 2019 Oct 21]. Available from: http://www.teses.usp.br/teses/disponiveis/9/9136/tde-01032013-092230/ ;.

Council of Science Editors:

Kimura TFE. Análise da capacidade migratória de células dendríticas na cromoblastomicose experimental. [Masters Thesis]. University of São Paulo; 2012. Available from: http://www.teses.usp.br/teses/disponiveis/9/9136/tde-01032013-092230/ ;

Temple University

8. Adhikary, Sabina. CANNABINOID RECEPTOR 2 AGONIST REDUCES IMMUNE CELL MIGRATION IN NEUROINFLAMMATION VIA INHIBITION OF MATRIX METALLOPROTEINASE-9.

Degree: PhD, 2013, Temple University

URL: http://digital.library.temple.edu/u?/p245801coll10,214799

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Physiology

Several studies have reported that administration of cannabinoid receptor agonists in inflammatory/autoimmune and CNS injury models resulted in significant attenuation of clinical disease. The… (more)

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Physiology

Several studies have reported that administration of cannabinoid receptor agonists in inflammatory/autoimmune and CNS injury models resulted in significant attenuation of clinical disease. The beneficial effects correlated with the observed reduction of inflammatory mediators and peripheral immune cell infiltration into the site of inflammation. Previous studies from our laboratories demonstrated that administration of cannabinoid type 2 receptor agonist attenuated disease score and improved recovery in two murine models of neuroinflammation; spinal cord injury (SCI) and experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis. The goal of the current investigation was to evaluate the mechanisms through which administration of selective cannabinoid-2 receptor (CB2R) agonists modify inflammatory responses and help to improve function in SCI and EAE. In SCI, an acute neuroinflammatory disorder, administration of CB2R agonist at 1 h and 24 h following contusion injury to the cord resulted in improved recovery of motor function and bladder function (the ability to spontaneously void) compared to control animals. Evaluation of inflammatory mediators at 48h demonstrated a dramatic reduction in the expression of the chemokines CXCL9, 10, 11 and cytokines IL-23 and its receptor in CB2R agonist-treated cords. There was also a reduction in the expression of toll-like receptors (TLR1, TLR4, TLR6, and TLR7), which correlated with a decreased number of immunoreactive microglia. Interestingly, at seven days post injury, CB2R agonist-treated injured cords showed a significant reduction in both hematopoietic and myeloid cell infiltration. In EAE, a chronic neuroinflammatory disorder, our laboratories demonstrated previously that administration of a CB2R agonist led to lower disease scores and improved recovery. In this study, we observed reduced numbers of infiltrating hematopoietic and myeloid cells into the spinal cord and brain of CB2 agonist-treated mice. This reduction was observed at the peak of disease (day 17) and the effect was maintained at the chronic stage of disease (day 30). Evaluation of molecules associated with cell migration showed decreased levels of the adhesion molecule VCAM-1 and matrix metalloproteinases MMP-2 and 9 at peak of EAE in treated mice. The decrease in VCAM-1 correlates with our previous observation of decreased leukocyte rolling and adhesion to brain microvasculature. However, the reduction in MMP-2/9 expression suggests that CB2R agonists may also affect leukocyte transmigration into the perivascular space and further infiltration into the CNS parenchyma. This process requires both chemokine cues and the gelatinases MMP2/9. Animals deficient in these MMPs show leukocyte accumulation in the perivascular space and are resistant to EAE. There are no reports in the literature on possible CB2R agonist effects on gelatinases in myeloid cells. Although both MMP-2 and -9 are produced by antigen-presenting cells and act on similar substrates, MMP-9 appears to play…

Advisors/Committee Members: Ganea, Doina, Autieri, Michael V., Tuma, Ronald F. (Ronald Franklin), Kilpatrick, Laurie, Rogers, Thomas J..

Subjects/Keywords: Immunology; Cannabinoid Receptor 2; Chemokines; Dendritic cell migration; Matrix Metalloproteinase 9; Multiple sclerosis; Spinal cord injury

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

APA (6^th Edition):

Adhikary, S. (2013). CANNABINOID RECEPTOR 2 AGONIST REDUCES IMMUNE CELL MIGRATION IN NEUROINFLAMMATION VIA INHIBITION OF MATRIX METALLOPROTEINASE-9. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,214799

Chicago Manual of Style (16^th Edition):

Adhikary, Sabina. “CANNABINOID RECEPTOR 2 AGONIST REDUCES IMMUNE CELL MIGRATION IN NEUROINFLAMMATION VIA INHIBITION OF MATRIX METALLOPROTEINASE-9.” 2013. Doctoral Dissertation, Temple University. Accessed October 21, 2019. http://digital.library.temple.edu/u?/p245801coll10,214799.

MLA Handbook (7^th Edition):

Adhikary, Sabina. “CANNABINOID RECEPTOR 2 AGONIST REDUCES IMMUNE CELL MIGRATION IN NEUROINFLAMMATION VIA INHIBITION OF MATRIX METALLOPROTEINASE-9.” 2013. Web. 21 Oct 2019.

Vancouver:

Adhikary S. CANNABINOID RECEPTOR 2 AGONIST REDUCES IMMUNE CELL MIGRATION IN NEUROINFLAMMATION VIA INHIBITION OF MATRIX METALLOPROTEINASE-9. [Internet] [Doctoral dissertation]. Temple University; 2013. [cited 2019 Oct 21]. Available from: http://digital.library.temple.edu/u?/p245801coll10,214799.

Council of Science Editors:

Adhikary S. CANNABINOID RECEPTOR 2 AGONIST REDUCES IMMUNE CELL MIGRATION IN NEUROINFLAMMATION VIA INHIBITION OF MATRIX METALLOPROTEINASE-9. [Doctoral Dissertation]. Temple University; 2013. Available from: http://digital.library.temple.edu/u?/p245801coll10,214799

9. Solanes, Paola. IP3 Receptor 3 controls migration persistency and environment patrolling by immature dendritic cells : Le récepteur IP3R-3 contrôle la persistance migratoire des cellules dendritiques immatures et leur capacité à explorer l’environnement.

Degree: Docteur es, Immunologie, 2013, Université Paris Descartes – Paris V

URL: http://www.theses.fr/2013PA05T020

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Le succès de la réponse immunitaire repose en grande partie sur la capacité des leucocytes à se déplacer et à accomplir leur fonction au sein… (more)

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Le succès de la réponse immunitaire repose en grande partie sur la capacité des leucocytes à se déplacer et à accomplir leur fonction au sein de structures anatomiques précises. Le fait qu’il puisse exister des mécanismes intrinsèques de coordination entre ces fonctions spécifiques et la migration de ces cellules n’a jamais été étudié auparavant. Nos travaux mettent en évidence, pour la première fois, l’existence d’un couplage entre la migration et la macropinocytose dans les cellules dendritiques qui explorent leur environnement en internalisant une grande quantité de matériel extra-cellulaire. C’est la Chaîne Invariante, protéine chaperon impliquée dans l’apprêtement des antigènes, qui est responsable de ce couplage en détournant le moteur Myosine II de l’arrière de la cellule, où elle promeut la migration, vers l’avant de la cellule. Ce recrutement transitoire de Myosin II autour des macropinosomes à l’avant favorise la macropinocytose et la délivrance de l’antigène dans les lysosomes, mais ralentit la cellule. L’implication de la Myosine II à la fois dans la migration et la capture d’antigène permet donc le couplage moléculaire entre ces deux processus et leur coordination spatio-temporelle. Cependant, les voies de signalisation impliquées dans le couplage avant/arrière dans les cellules dendritiques immatures restent encore méconnues. L’ensemble de mes travaux de thèse montrent que la libération de calcium du réticulum endoplasmique à travers les récepteurs IP3 (IP3Rs) est nécessaire pour maintenir le niveau de phosphorylation de la chaîne légère de Myosin (MLC) et la polarisation avant/arrière de Myosine II au cours de la migration des cellules dendritiques immatures. Nous montrons que les récepteurs IP3R1, 2 et 3 sont requis pour atteindre une vitesse maximale en 2- et 3-Dimension, et que le récepteur IP3R3, et dans une moindre mesure IP3R1, favorisent la persistance des cellules. En revanche, l’inhibition de l’expression du récepteur IP3R3 augmente la capacité des cellules dendritiques immatures à capturer l’antigène, ce qui est en accord avec notre résultat montrant que la capture de l'antigène est inversement reliée à la locomotion de cellules dendritiques. Nous proposons que le relargage du calcium par le réticulum endoplasmique favorise l’activité de la myosine II ce qui permet aux cellules dendritiques de ralentir de façon transitoire. Ce relargage calcique permet aux cellules dendritiques du optimiser l'internalisation des antigènes extracellulaires en maintenant leur polarité ce qui leur permet d’optimiser ainsi leur capacité d'échantillonnage de l’environnement.

The immune response heavily relies on the migration capacity of leukocytes. These cells must stop in precise anatomical locations to fulfill a particular task. But whether and how specific functions are coordinated with migration by cell-intrinsic mechanisms is not known. We here show that in dendritic cells, which patrol their environment for the presence of antigens by internalizing extracellular material, macropinocytosis is coupled to…

Advisors/Committee Members: Lennon-Dumenil, Ana-Maria (thesis director).

Subjects/Keywords: Migration cellulaire; Canaux calciques; Myosine II; Capture et présentation d’antigène; Cellules dendritiques; Cell migration; Calcium channels; Myosin II; Antigen capture and presentation; Dendritic cells; 616.079

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

APA (6^th Edition):

Solanes, P. (2013). IP3 Receptor 3 controls migration persistency and environment patrolling by immature dendritic cells : Le récepteur IP3R-3 contrôle la persistance migratoire des cellules dendritiques immatures et leur capacité à explorer l’environnement. (Doctoral Dissertation). Université Paris Descartes – Paris V. Retrieved from http://www.theses.fr/2013PA05T020

Chicago Manual of Style (16^th Edition):

Solanes, Paola. “IP3 Receptor 3 controls migration persistency and environment patrolling by immature dendritic cells : Le récepteur IP3R-3 contrôle la persistance migratoire des cellules dendritiques immatures et leur capacité à explorer l’environnement.” 2013. Doctoral Dissertation, Université Paris Descartes – Paris V. Accessed October 21, 2019. http://www.theses.fr/2013PA05T020.

MLA Handbook (7^th Edition):

Solanes, Paola. “IP3 Receptor 3 controls migration persistency and environment patrolling by immature dendritic cells : Le récepteur IP3R-3 contrôle la persistance migratoire des cellules dendritiques immatures et leur capacité à explorer l’environnement.” 2013. Web. 21 Oct 2019.

Vancouver:

Solanes P. IP3 Receptor 3 controls migration persistency and environment patrolling by immature dendritic cells : Le récepteur IP3R-3 contrôle la persistance migratoire des cellules dendritiques immatures et leur capacité à explorer l’environnement. [Internet] [Doctoral dissertation]. Université Paris Descartes – Paris V; 2013. [cited 2019 Oct 21]. Available from: http://www.theses.fr/2013PA05T020.

Council of Science Editors:

Solanes P. IP3 Receptor 3 controls migration persistency and environment patrolling by immature dendritic cells : Le récepteur IP3R-3 contrôle la persistance migratoire des cellules dendritiques immatures et leur capacité à explorer l’environnement. [Doctoral Dissertation]. Université Paris Descartes – Paris V; 2013. Available from: http://www.theses.fr/2013PA05T020

10. Chabaud, Mélanie. Cell migration and antigen uptake are two antagonistic functions that are coupled by Myosin II in dendritic cells : La migration cellulaire et la capture d'antigènes sont des fonctions antagonistes couplées par la Myosine II dans les cellules dendritiques.

Degree: Docteur es, Biologie cellulaire, 2014, Université Paris Descartes – Paris V

URL: http://www.theses.fr/2014PA05T021

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Les cellules dendritiques (DCs) patrouillent les tissus périphériques à la recherche de dangers potentiels en se déplaçant à travers les tissus et en incorporant de… (more)

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Les cellules dendritiques (DCs) patrouillent les tissus périphériques à la recherche de dangers potentiels en se déplaçant à travers les tissus et en incorporant de grande quantité de matériel extracellulaire. Cet événement précoce de la réponse immunitaire adaptative est susceptible de déterminer l'amplitude et la qualité de l'activation des lymphocytes T et B. De ce fait, les DCs pourraient avoir besoin d'orchestrer leur motilité et leur fonction de capture des antigènes afin d'initier un réponse immunitaire efficace et adaptée. Afin d'étudier les mécanismes responsables de l'optimisation de l'échantillonnage des tissus par les DCs, nous avons suivi leur migration et leur capacité à capturer des antigènes dans des chambres micro-fluidiques contenant des canaux étroits qui permettent de reproduire l'espace confiné des tissus périphériques. De manière surprenante, nous avons découvert que la migration des DCs et leur aptitude à accumuler des antigènes sont des fonctions antagonistes et dépendent de l'activité du moteur moléculaire Myosine II. Nous avons observé que les DCs se déplacent en alternant des phases rapides au cours desquelles la Myosine II est distribuée de manière asymétrique à l'arrière des cellules, et des phases plus lentes pendant lesquelles la Myosine II est enrichie à l'avant. Les enrichissements transitoires de Myosine II à l'avant des DCs dépendent de l'association de la Myosine II avec la chaîne invariante associée au CMH-II (Ii). Ces évenements favorisent l'absorption d'antigènes et leur transport dans les compartiments endolysosomaux. Des expériences menées avec une pince optique nous ont permis de montrer que l'activité de la Myosine II à l'avant des cellules génère des forces mécaniques qui induisent le transport des vésicules vers l'intérieur de la cellule, probablement en modulant le flux rétrograde d'actine. Ainsi, au cours de cette thèse, nous avons montré que la Myosine II était nécessaire à la fois pour la migration cellulaire et la capture d'antigènes, établissant un mécanisme moléculaire qui permet de coordonner ces deux processus dans le temps et l'espace. Nous proposons que l'alternance de phases de haute mobilité et de phases d'arrêt associées à la capture d'antigènes confère aux DCs une stratégie de recherche intermittente qui leur permettrait d'optimiser la surveillance des tissus périphériques.

Dendritic cells (DCs) patrol peripheral tissues in search for potential dangers by actively crawling and internalizing extracellular materiel. This initial event of an adaptive immune response is likely to determine the magnitude and quality of T cell and B cell immunity. Therefore, DCs might need to tightly orchestrate their migration and their antigen uptake function in order to mount an efficient and adapted immune response. To investigate the mechanisms responsible for the optimization of tissues sampling by DCs, we monitored their migration and their ability to capture antigens in micro-fluidic chambers containing narrow channels that mimic the confined space of peripheral…

Advisors/Committee Members: Lennon-Dumenil, Ana-Maria (thesis director), Piel, Matthieu (thesis director).

Subjects/Keywords: Migration cellulaire; Macropinocytose; Myosine II; Chaine Invariante (CD74); Trafic endocytique; Capture d'antigènes; Cellules dendritiques; Cell Migration; Macropinocytosis; Myosin II; Invariant Chain (CD74); Endocytic trafficking; Antigen capture; Dendritic cells; 571.964 5

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

APA (6^th Edition):

Chabaud, M. (2014). Cell migration and antigen uptake are two antagonistic functions that are coupled by Myosin II in dendritic cells : La migration cellulaire et la capture d'antigènes sont des fonctions antagonistes couplées par la Myosine II dans les cellules dendritiques. (Doctoral Dissertation). Université Paris Descartes – Paris V. Retrieved from http://www.theses.fr/2014PA05T021

Chicago Manual of Style (16^th Edition):

Chabaud, Mélanie. “Cell migration and antigen uptake are two antagonistic functions that are coupled by Myosin II in dendritic cells : La migration cellulaire et la capture d'antigènes sont des fonctions antagonistes couplées par la Myosine II dans les cellules dendritiques.” 2014. Doctoral Dissertation, Université Paris Descartes – Paris V. Accessed October 21, 2019. http://www.theses.fr/2014PA05T021.

MLA Handbook (7^th Edition):

Chabaud, Mélanie. “Cell migration and antigen uptake are two antagonistic functions that are coupled by Myosin II in dendritic cells : La migration cellulaire et la capture d'antigènes sont des fonctions antagonistes couplées par la Myosine II dans les cellules dendritiques.” 2014. Web. 21 Oct 2019.

Vancouver:

Chabaud M. Cell migration and antigen uptake are two antagonistic functions that are coupled by Myosin II in dendritic cells : La migration cellulaire et la capture d'antigènes sont des fonctions antagonistes couplées par la Myosine II dans les cellules dendritiques. [Internet] [Doctoral dissertation]. Université Paris Descartes – Paris V; 2014. [cited 2019 Oct 21]. Available from: http://www.theses.fr/2014PA05T021.

Council of Science Editors:

Chabaud M. Cell migration and antigen uptake are two antagonistic functions that are coupled by Myosin II in dendritic cells : La migration cellulaire et la capture d'antigènes sont des fonctions antagonistes couplées par la Myosine II dans les cellules dendritiques. [Doctoral Dissertation]. Université Paris Descartes – Paris V; 2014. Available from: http://www.theses.fr/2014PA05T021

11. Otten, Marielle Anna. Antibody therapeutic approaches for cancer.

Degree: 2006, University Utrecht

URL: http://dspace.library.uu.nl/handle/1874/9465 ; URN:NBN:NL:UI:10-1874-9465 ; urn:isbn:90-8559-171-6 ; URN:NBN:NL:UI:10-1874-9465 ; http://dspace.library.uu.nl/handle/1874/9465

► FcalphaRI as target for antibody therapy: Anti-tumor antibodies are promising therapeutics for cancer. Currently, all FDA-approved therapeutic antibodies are of the IgG class, which interact… (more)

▼ FcalphaRI as target for antibody therapy: Anti-tumor antibodies are promising therapeutics for cancer. Currently, all FDA-approved therapeutic antibodies are of the IgG class, which interact with IgG receptors (FcgammaR). In this project we examined the role of the IgA Fc receptor, FcalphaRI (CD89) in antibody therapy. Antibody-induced neutrophil migration was studied in 3-dimensional collagen culture assays, in which tumor-colonies were grown. Minimal tumor-directed neutrophil migration was induced by IgG anti-tumor antibodies. In contrast, FcalphaRI triggered massive neutrophil migration and tumor-colony destruction. Production of chemotactic factors and release of inflammatory cytokines were increased, as well, suggesting an FcalphaRI-induced autocrine loop, leading to neutrophil migration and consequent destruction of tumor-colonies. In addition, tumor-cell killing was consistently more effective via triggering of FcalphaRI, than via FcgammaRI. Taken together, neutrophil FcalphaRI might represent an effective target for antibody therapy. Successful antibody therapy against liver-metastases: In colorectal cancer, many patients will develop liver-metastases, even after successful surgical removal of the primary tumor at a time at which no visible metastases are present. Peri-operative adjuvant treatment might, therefore, help to prevent secondary disease. We studied the potential of antibody-therapy to prevent outgrowth of liver-metastases in mice. Peri-operative treatment with anti-gp75 IgG2a prevented outgrowth of B16F10 liver-metastases in more than 90% of mice. Therapeutic efficacy was maintained in either C1q-, or CR3-deficient mice, but was abrogated in FcRgamma chain-deficient mice, which lack all activatory FcgammaR. These results indicate that interactions with activatory FcgammaR are necessary for successful antibody therapy of cancer. Because antibody therapy was still effective in FcgammaRI-/-, FcgammaRIII-/- and FcgammaRI/III-/- mice, an important role for the newly identified FcgammaRIV is supported.

Subjects/Keywords: Fc receptor; antibody; FcalphaRI; FcgammaR; immunotherapy; neutrophil; dendritic cell; migration; tumor; liver metastases

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

APA (6^th Edition):

Otten, M. A. (2006). Antibody therapeutic approaches for cancer. (Doctoral Dissertation). University Utrecht. Retrieved from http://dspace.library.uu.nl/handle/1874/9465 ; URN:NBN:NL:UI:10-1874-9465 ; urn:isbn:90-8559-171-6 ; URN:NBN:NL:UI:10-1874-9465 ; http://dspace.library.uu.nl/handle/1874/9465

Chicago Manual of Style (16^th Edition):

Otten, Marielle Anna. “Antibody therapeutic approaches for cancer.” 2006. Doctoral Dissertation, University Utrecht. Accessed October 21, 2019. http://dspace.library.uu.nl/handle/1874/9465 ; URN:NBN:NL:UI:10-1874-9465 ; urn:isbn:90-8559-171-6 ; URN:NBN:NL:UI:10-1874-9465 ; http://dspace.library.uu.nl/handle/1874/9465.

MLA Handbook (7^th Edition):

Otten, Marielle Anna. “Antibody therapeutic approaches for cancer.” 2006. Web. 21 Oct 2019.

Vancouver:

Otten MA. Antibody therapeutic approaches for cancer. [Internet] [Doctoral dissertation]. University Utrecht; 2006. [cited 2019 Oct 21]. Available from: http://dspace.library.uu.nl/handle/1874/9465 ; URN:NBN:NL:UI:10-1874-9465 ; urn:isbn:90-8559-171-6 ; URN:NBN:NL:UI:10-1874-9465 ; http://dspace.library.uu.nl/handle/1874/9465.

Council of Science Editors:

Otten MA. Antibody therapeutic approaches for cancer. [Doctoral Dissertation]. University Utrecht; 2006. Available from: http://dspace.library.uu.nl/handle/1874/9465 ; URN:NBN:NL:UI:10-1874-9465 ; urn:isbn:90-8559-171-6 ; URN:NBN:NL:UI:10-1874-9465 ; http://dspace.library.uu.nl/handle/1874/9465

12. Otten, Marielle Anna. Antibody therapeutic approaches for cancer.

Degree: 2006, University Utrecht

URL: http://dspace.library.uu.nl/handle/1874/9465 ; URN:NBN:NL:UI:10-1874-9465 ; urn:isbn:90-8559-171-6 ; URN:NBN:NL:UI:10-1874-9465 ; http://dspace.library.uu.nl/handle/1874/9465

► FcalphaRI as target for antibody therapy: Anti-tumor antibodies are promising therapeutics for cancer. Currently, all FDA-approved therapeutic antibodies are of the IgG class, which interact… (more)

▼ FcalphaRI as target for antibody therapy: Anti-tumor antibodies are promising therapeutics for cancer. Currently, all FDA-approved therapeutic antibodies are of the IgG class, which interact with IgG receptors (FcgammaR). In this project we examined the role of the IgA Fc receptor, FcalphaRI (CD89) in antibody therapy. Antibody-induced neutrophil migration was studied in 3-dimensional collagen culture assays, in which tumor-colonies were grown. Minimal tumor-directed neutrophil migration was induced by IgG anti-tumor antibodies. In contrast, FcalphaRI triggered massive neutrophil migration and tumor-colony destruction. Production of chemotactic factors and release of inflammatory cytokines were increased, as well, suggesting an FcalphaRI-induced autocrine loop, leading to neutrophil migration and consequent destruction of tumor-colonies. In addition, tumor-cell killing was consistently more effective via triggering of FcalphaRI, than via FcgammaRI. Taken together, neutrophil FcalphaRI might represent an effective target for antibody therapy. Successful antibody therapy against liver-metastases: In colorectal cancer, many patients will develop liver-metastases, even after successful surgical removal of the primary tumor at a time at which no visible metastases are present. Peri-operative adjuvant treatment might, therefore, help to prevent secondary disease. We studied the potential of antibody-therapy to prevent outgrowth of liver-metastases in mice. Peri-operative treatment with anti-gp75 IgG2a prevented outgrowth of B16F10 liver-metastases in more than 90% of mice. Therapeutic efficacy was maintained in either C1q-, or CR3-deficient mice, but was abrogated in FcRgamma chain-deficient mice, which lack all activatory FcgammaR. These results indicate that interactions with activatory FcgammaR are necessary for successful antibody therapy of cancer. Because antibody therapy was still effective in FcgammaRI-/-, FcgammaRIII-/- and FcgammaRI/III-/- mice, an important role for the newly identified FcgammaRIV is supported.

Subjects/Keywords: Fc receptor; antibody; FcalphaRI; FcgammaR; immunotherapy; neutrophil; dendritic cell; migration; tumor; liver metastases

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Otten, M. A. (2006). Antibody therapeutic approaches for cancer. (Doctoral Dissertation). University Utrecht. Retrieved from http://dspace.library.uu.nl/handle/1874/9465 ; URN:NBN:NL:UI:10-1874-9465 ; urn:isbn:90-8559-171-6 ; URN:NBN:NL:UI:10-1874-9465 ; http://dspace.library.uu.nl/handle/1874/9465

Chicago Manual of Style (16^th Edition):

Otten, Marielle Anna. “Antibody therapeutic approaches for cancer.” 2006. Doctoral Dissertation, University Utrecht. Accessed October 21, 2019. http://dspace.library.uu.nl/handle/1874/9465 ; URN:NBN:NL:UI:10-1874-9465 ; urn:isbn:90-8559-171-6 ; URN:NBN:NL:UI:10-1874-9465 ; http://dspace.library.uu.nl/handle/1874/9465.

MLA Handbook (7^th Edition):

Otten, Marielle Anna. “Antibody therapeutic approaches for cancer.” 2006. Web. 21 Oct 2019.

Vancouver:

Otten MA. Antibody therapeutic approaches for cancer. [Internet] [Doctoral dissertation]. University Utrecht; 2006. [cited 2019 Oct 21]. Available from: http://dspace.library.uu.nl/handle/1874/9465 ; URN:NBN:NL:UI:10-1874-9465 ; urn:isbn:90-8559-171-6 ; URN:NBN:NL:UI:10-1874-9465 ; http://dspace.library.uu.nl/handle/1874/9465.

Council of Science Editors:

Otten MA. Antibody therapeutic approaches for cancer. [Doctoral Dissertation]. University Utrecht; 2006. Available from: http://dspace.library.uu.nl/handle/1874/9465 ; URN:NBN:NL:UI:10-1874-9465 ; urn:isbn:90-8559-171-6 ; URN:NBN:NL:UI:10-1874-9465 ; http://dspace.library.uu.nl/handle/1874/9465

University of Oxford

13. Giblin, Sean. Investigating cell lineage specific biosynthesis of tenascin-C during inflammation.

Degree: PhD, 2018, University of Oxford

URL: http://ora.ox.ac.uk/objects/uuid:8c7306d8-53cf-4131-a134-f74885e37cc9 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.748981

► The extracellular matrix (ECM) is a complex network of molecules secreted by cells, which is essential for providing structural support and facilitating cell processes including… (more)

▼ The extracellular matrix (ECM) is a complex network of molecules secreted by cells, which is essential for providing structural support and facilitating cell processes including adhesion, migration and survival. Tenascin-C is an immunomodulatory ECM protein that exhibits limited expression in healthy tissues, but is transiently elevated at sites of tissue injury, and is persistently expressed in chronic inflammatory diseases and tumours. Alternative splicing of 9 of tenascin-C's fibronectin type III-like domains (FnIII- A1, A2, A3, A4, B, AD2, AD1, C and D) generates enormous diversity in form; yielding 511 possible isoforms. Post-transcriptional modification of tenascin-C has been studied in cancer and during development where disease and tissue specific isoforms exhibit distinct adhesive, migratory and proliferative effects. However, little is known of how tenascin-C is expressed or alternatively spliced during inflammation. This study characterises inflammation and disease specific tenascin-C isoforms made by immune cells and fibroblasts, and investigates their functional relevance. Biosynthesis and alternative splicing of tenascin-C was examined using standard curve qPCR, ELISA, Western blot and confocal immunocytochemistry in resting and activated primary human immune cells, dermal fibroblasts, and in synovial fibroblasts isolated from healthy controls and from osteoarthritis (OA) and rheumatoid arthritis (RA) patients. Based on these data, three recombinant proteins comprising FnIII domains AD2-AD1, B-C-D and B-AD2-AD1-C-D were cloned, expressed and purified, and their impact on cell behaviour including adhesion, morphology and migration was assessed. Basal tenascin-C expression was lower in myeloid and lymphoid cells than fibroblasts, and was induced in all following inflammatory stimulation. Tenascin-C expression was elevated in disease with RA and OA synovial fibroblasts containing higher levels than healthy controls. Alternative splicing following cell activation was cell-type specific: all FnIII except AD2 and AD1 were upregulated in dendritic cells and macrophages, in T-cells all FnIII remained unchanged with FnIII A1 absent; and no change in splicing was observed in activated dermal fibroblasts. Normal and OA synovial fibroblasts exhibited similar tenascin-C splicing patterns, but FnIII B and D were specifically elevated in RA. Functional analysis revealed differences in the adhesion, morphology and migration of myeloid cells and dermal fibroblasts cultured on FnIII AD2-AD1, B-C-D, B-AD2-AD1-C-D and full length tenascin-C substrates; FnIII B-C-D promoted MDDC migration while B-AD2-AD1-C-D promoted fibroblast adhesion, compared to full length tenascin-C. For the first time, this study reveals differences in tenascin-C biosynthesis and alternative splicing by immune cells and fibroblasts following activation with inflammatory stimuli; and starts to reveal how alternative splicing of tenascin-C may influence the behaviours of both stromal and immune cells types during inflammation and in inflammatory…

Subjects/Keywords: Cell biology; Alternative splicing; Extracellular matrix biology; Immunology; Protein biochemistry; FnIII; Cell migration; Fibroblasts; Alternative RNA splicing; Dendritic cells; Tenascin-C; Fibronectin type 3-like domains; Extracellular Matrix; Macrophages; Lymphocytes; standard curve qPCR; Cell adhesion; Primary human immune cells; Cytokine

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

APA (6^th Edition):

Giblin, S. (2018). Investigating cell lineage specific biosynthesis of tenascin-C during inflammation. (Doctoral Dissertation). University of Oxford. Retrieved from http://ora.ox.ac.uk/objects/uuid:8c7306d8-53cf-4131-a134-f74885e37cc9 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.748981

Chicago Manual of Style (16^th Edition):

Giblin, Sean. “Investigating cell lineage specific biosynthesis of tenascin-C during inflammation.” 2018. Doctoral Dissertation, University of Oxford. Accessed October 21, 2019. http://ora.ox.ac.uk/objects/uuid:8c7306d8-53cf-4131-a134-f74885e37cc9 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.748981.

MLA Handbook (7^th Edition):

Giblin, Sean. “Investigating cell lineage specific biosynthesis of tenascin-C during inflammation.” 2018. Web. 21 Oct 2019.

Vancouver:

Giblin S. Investigating cell lineage specific biosynthesis of tenascin-C during inflammation. [Internet] [Doctoral dissertation]. University of Oxford; 2018. [cited 2019 Oct 21]. Available from: http://ora.ox.ac.uk/objects/uuid:8c7306d8-53cf-4131-a134-f74885e37cc9 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.748981.

Council of Science Editors:

Giblin S. Investigating cell lineage specific biosynthesis of tenascin-C during inflammation. [Doctoral Dissertation]. University of Oxford; 2018. Available from: http://ora.ox.ac.uk/objects/uuid:8c7306d8-53cf-4131-a134-f74885e37cc9 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.748981

Universiteit Utrecht

14. Otten, Marielle Anna. Antibody therapeutic approaches for cancer.

Degree: 2006, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/9465

► FcalphaRI as target for antibody therapy: Anti-tumor antibodies are promising therapeutics for cancer. Currently, all FDA-approved therapeutic antibodies are of the IgG class, which interact… (more)

▼ FcalphaRI as target for antibody therapy: Anti-tumor antibodies are promising therapeutics for cancer. Currently, all FDA-approved therapeutic antibodies are of the IgG class, which interact with IgG receptors (FcgammaR). In this project we examined the role of the IgA Fc receptor, FcalphaRI (CD89) in antibody therapy. Antibody-induced neutrophil migration was studied in 3-dimensional collagen culture assays, in which tumor-colonies were grown. Minimal tumor-directed neutrophil migration was induced by IgG anti-tumor antibodies. In contrast, FcalphaRI triggered massive neutrophil migration and tumor-colony destruction. Production of chemotactic factors and release of inflammatory cytokines were increased, as well, suggesting an FcalphaRI-induced autocrine loop, leading to neutrophil migration and consequent destruction of tumor-colonies. In addition, tumor-cell killing was consistently more effective via triggering of FcalphaRI, than via FcgammaRI. Taken together, neutrophil FcalphaRI might represent an effective target for antibody therapy. Successful antibody therapy against liver-metastases: In colorectal cancer, many patients will develop liver-metastases, even after successful surgical removal of the primary tumor at a time at which no visible metastases are present. Peri-operative adjuvant treatment might, therefore, help to prevent secondary disease. We studied the potential of antibody-therapy to prevent outgrowth of liver-metastases in mice. Peri-operative treatment with anti-gp75 IgG2a prevented outgrowth of B16F10 liver-metastases in more than 90% of mice. Therapeutic efficacy was maintained in either C1q-, or CR3-deficient mice, but was abrogated in FcRgamma chain-deficient mice, which lack all activatory FcgammaR. These results indicate that interactions with activatory FcgammaR are necessary for successful antibody therapy of cancer. Because antibody therapy was still effective in FcgammaRI-/-, FcgammaRIII-/- and FcgammaRI/III-/- mice, an important role for the newly identified FcgammaRIV is supported.

Subjects/Keywords: Geneeskunde; Fc receptor; antibody; FcalphaRI; FcgammaR; immunotherapy; neutrophil; dendritic cell; migration; tumor; liver metastases

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

APA (6^th Edition):

Otten, M. A. (2006). Antibody therapeutic approaches for cancer. (Doctoral Dissertation). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/9465

Chicago Manual of Style (16^th Edition):

Otten, Marielle Anna. “Antibody therapeutic approaches for cancer.” 2006. Doctoral Dissertation, Universiteit Utrecht. Accessed October 21, 2019. http://dspace.library.uu.nl:8080/handle/1874/9465.

MLA Handbook (7^th Edition):

Otten, Marielle Anna. “Antibody therapeutic approaches for cancer.” 2006. Web. 21 Oct 2019.

Vancouver:

Otten MA. Antibody therapeutic approaches for cancer. [Internet] [Doctoral dissertation]. Universiteit Utrecht; 2006. [cited 2019 Oct 21]. Available from: http://dspace.library.uu.nl:8080/handle/1874/9465.

Council of Science Editors:

Otten MA. Antibody therapeutic approaches for cancer. [Doctoral Dissertation]. Universiteit Utrecht; 2006. Available from: http://dspace.library.uu.nl:8080/handle/1874/9465

15. GE QING. Interplay of innate and adaptive systems in influenza A infection and Pulmonary Inflammation: Role of Natural Killer cells.

Degree: 2014, National University of Singapore

URL: http://scholarbank.nus.edu.sg/handle/10635/80182

Subjects/Keywords: Natural killer cells; Dendritic cells migration; IFN-g; SP-D; CTL; T cell recruitment

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

APA (6^th Edition):

QING, G. (2014). Interplay of innate and adaptive systems in influenza A infection and Pulmonary Inflammation: Role of Natural Killer cells. (Thesis). National University of Singapore. Retrieved from http://scholarbank.nus.edu.sg/handle/10635/80182

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):

QING, GE. “Interplay of innate and adaptive systems in influenza A infection and Pulmonary Inflammation: Role of Natural Killer cells.” 2014. Thesis, National University of Singapore. Accessed October 21, 2019. http://scholarbank.nus.edu.sg/handle/10635/80182.

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

MLA Handbook (7^th Edition):

QING, GE. “Interplay of innate and adaptive systems in influenza A infection and Pulmonary Inflammation: Role of Natural Killer cells.” 2014. Web. 21 Oct 2019.

Vancouver:

QING G. Interplay of innate and adaptive systems in influenza A infection and Pulmonary Inflammation: Role of Natural Killer cells. [Internet] [Thesis]. National University of Singapore; 2014. [cited 2019 Oct 21]. Available from: http://scholarbank.nus.edu.sg/handle/10635/80182.

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

Council of Science Editors:

QING G. Interplay of innate and adaptive systems in influenza A infection and Pulmonary Inflammation: Role of Natural Killer cells. [Thesis]. National University of Singapore; 2014. Available from: http://scholarbank.nus.edu.sg/handle/10635/80182

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

ETH Zürich

16. Russo, Erica. Interactions between Lymphatic Vessels and Leukocytes: Elucidating their impact on lymphatic function and immunity.

Degree: 2016, ETH Zürich

URL: http://hdl.handle.net/20.500.11850/155752

Subjects/Keywords: LYMPHE + LYMPHSYSTEM + RETIKULO-ENDOTHELIALES SYSTEM (ANATOMIE UND PHYSIOLOGIE); GEFÄSSWAND-ENDOTHEL (ANATOMIE, HISTOLOGIE, PHYSIOLOGIE); LEUKOZYTEN + AMÖBOIDE BLUTZELLEN (BLUTZELLEN); DENDRITISCHE ZELLEN (IMMUNOLOGIE); ZELLWANDERUNG (CYTOLOGISCHE HISTOLOGIE); IMMUNREAKTION + IMMUNANTWORT (IMMUNOLOGIE); LYMPH + LYMPHATIC SYSTEM + RETICULO-ENDOTHELIAL SYSTEM (ANATOMY AND PHYSIOLOGY); VASCULAR ENDOTHELIUM (ANATOMY, HISTOLOGY, PHYSIOLOGY); LEUKOCYTES + AMOEBOID BLOOD CELLS (BLOOD CELLS); DENDRITIC CELLS (IMMUNOLOGY); CELL MIGRATION (CYTOLOGICAL HISTOLOGY); IMMUNE REACTION + IMMUNE RESPONSE (IMMUNOLOGY); info:eu-repo/classification/ddc/610; Medical sciences, medicine

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

APA (6^th Edition):

Russo, E. (2016). Interactions between Lymphatic Vessels and Leukocytes: Elucidating their impact on lymphatic function and immunity. (Doctoral Dissertation). ETH Zürich. Retrieved from http://hdl.handle.net/20.500.11850/155752

Chicago Manual of Style (16^th Edition):

Russo, Erica. “Interactions between Lymphatic Vessels and Leukocytes: Elucidating their impact on lymphatic function and immunity.” 2016. Doctoral Dissertation, ETH Zürich. Accessed October 21, 2019. http://hdl.handle.net/20.500.11850/155752.

MLA Handbook (7^th Edition):

Russo, Erica. “Interactions between Lymphatic Vessels and Leukocytes: Elucidating their impact on lymphatic function and immunity.” 2016. Web. 21 Oct 2019.

Vancouver:

Russo E. Interactions between Lymphatic Vessels and Leukocytes: Elucidating their impact on lymphatic function and immunity. [Internet] [Doctoral dissertation]. ETH Zürich; 2016. [cited 2019 Oct 21]. Available from: http://hdl.handle.net/20.500.11850/155752.

Council of Science Editors:

Russo E. Interactions between Lymphatic Vessels and Leukocytes: Elucidating their impact on lymphatic function and immunity. [Doctoral Dissertation]. ETH Zürich; 2016. Available from: http://hdl.handle.net/20.500.11850/155752

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