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25 results on '"Clay, Bryan S."'

2. Abstract 5617: A novel genetically modified oncolytic vaccinia virus selectively replicates in tumors to activate an inflammatory TME and induce tumor regression

Author

Goenaga, Anne-Laure, primary, Wang, I-Ming, additional, Clay, Bryan S., additional, Lang, Susanne, additional, Wang, Annabel, additional, Weady, Peter, additional, Pillai, Smitha P.S., additional, Ram, Sripad, additional, Mitchell, Leah, additional, Eisenbraun, Michael, additional, Binder, Joseph, additional, Avidal, Liliana Maruri, additional, Kirn, David, additional, Hollingsworth, Robert, additional, and Lees, Clare, additional

Published
2022
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4. IL-33--dependent induction of allergic lung inflammation by FcγRIII signaling

Author

Tjota, Melissa Y., Williams, Jesse W., Lu, Tiffany, Clay, Bryan S., Byrd, Tiara, Hrusch, Cara L., Decker, Donna C., de Araujo, Claudia Alves, Bryce, Paul J., and Sperling, Anne I.

Subjects
Inflammation -- Research -- Genetic aspects -- Development and progression, Cellular signal transduction -- Research -- Physiological aspects, Interleukins -- Research -- Physiological aspects, Asthma -- Research -- Genetic aspects, Health care industry
Abstract

Atopic asthma is a chronic inflammatory disease of the lungs generally marked by excessive Th2 inflammation. The role of allergen-specific IgG in asthma is still controversial; however, a receptor of [...]

Published
2013
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9. ICOS Costimulation Expands Th2 Immunity by Augmenting Migration of Lymphocytes to Draining Lymph Nodes1

Author

Tesciuba, Amanda G., Shilling, Rebecca A., Agarwal, Monica D., Bandukwala, Hozefa S., Clay, Bryan S., Moore, Tamson V., Weinstock, Joel V., Welcher, Andrew A., and Sperling, Anne I.

Subjects
Antigens, Differentiation, T-Lymphocyte, Mice, Knockout, B-Lymphocytes, T-Lymphocytes, Mice, Transgenic, Schistosoma mansoni, Article, Inducible T-Cell Co-Stimulator Protein, Mice, Inbred C57BL, Inducible T-Cell Co-Stimulator Ligand, Mice, Th2 Cells, Cell Movement, B7-1 Antigen, Animals, Cytokines, Female, Lymph Nodes, Lymphocytes
Abstract

The T cell costimulatory molecule ICOS regulates Th2 effector function in allergic airway disease. Recently, several studies with ICOS−/− mice have also demonstrated a role for ICOS in Th2 differentiation. To determine the effects of ICOS on the early immune response, we investigated augmenting ICOS costimulation in a Th2-mediated immune response to Schistosoma mansoni antigens. We found that augmenting ICOS costimulation with B7RP-1-Fc increased the accumulation of T and B cells in the draining lymph nodes post-immunization. Interestingly, the increased numbers were due in part to increased migration of undivided antigen-specific TCR transgenic T cells and surprisingly B cells, as well as non-TCR transgenic T cells. B7RP-1-Fc also increased the levels of the chemokines, CCL21 and CXCL13, in the draining lymph node, suggesting ICOS costimulation contributes to migration by direct or indirect effects on, dendritic cells, stromal cells and high endothelial venules. Further, the effects of B7RP-1-Fc were not dependent on immunization. Our data support a model in which ICOS costimulation augments the pool of lymphocytes in the draining lymph nodes leading to an increase in the frequency of potentially reactive T and B cells.

Published
2008

10. CD43 Regulates Th2 Differentiation and Inflammation1

Author

Cannon, Judy L., Collins, Amélie, Mody, Purvi D., Balachandran, Diwaker, Henriksen, Kammi J., Smith, Cassandra E., Tong, Jiankun, Clay, Bryan S., Miller, Stephen D., and Sperling, Anne I.

Subjects
Cell Nucleus, Inflammation, Leukosialin, Receptors, Antigen, T-Cell, hemic and immune systems, Autoimmunity, Cell Differentiation, GATA3 Transcription Factor, Immunoglobulin E, Th1 Cells, Article, Mice, Mutant Strains, Mice, Th2 Cells, immune system diseases, Mice, Inbred NOD, T-Lymphocyte Subsets, hemic and lymphatic diseases, Respiratory Hypersensitivity, Animals, Calcium, Interleukin-4, Interleukin-5, Cells, Cultured, Cell Proliferation
Abstract

CD43 is a highly glycosylated transmembrane protein that regulates T cell activation. CD43(-/-) T cells are hyperproliferative and the cytoplasmic tail of CD43 has been found to be sufficient to reconstitute wild-type proliferation levels, suggesting an intracellular mechanism. In this study, we report that upon TCR ligation CD43(-/-) T cells demonstrated no increase in tyrosine phosphorylation but a decreased calcium flux. Interestingly, CD43(-/-) T cells preferentially differentiated into Th2 cells in vitro, and CD43(-/-) T cells show increased GATA-3 translocation into the nucleus. In vivo, CD43(-/-) mice exhibited increased inflammation in two separate models of Th2-mediated allergic airway disease. In contrast, in Th1-mediated diabetes, nonobese diabetic CD43(-/-) mice did not significantly differ from wild-type mice in disease onset or progression. Th1-induced experimental autoimmune encephalomyelitis to MOG(35-55) was also normal in the CD43(-/-) mice. Nonetheless, the CD43(-/-) mice produced more IL-5 when restimulated with MOG(35-55) in vitro and demonstrated decreased delayed-type hypersensitivity responses. Together, these data demonstrate that although CD43(-/-) T cells preferentially differentiate into Th2 cells, this response is not sufficient to protect against Th1-mediated autoimmune responses.

Published
2008

11. Transcription factor IRF4 drives dendritic cells to promote Th2 differentiation

Author

Williams, Jesse W., primary, Tjota, Melissa Y., additional, Clay, Bryan S., additional, Vander Lugt, Bryan, additional, Bandukwala, Hozefa S., additional, Hrusch, Cara L., additional, Decker, Donna C., additional, Blaine, Kelly M., additional, Fixsen, Bethany R., additional, Singh, Harinder, additional, Sciammas, Roger, additional, and Sperling, Anne I., additional

Published
2013
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12. ICOS-Expressing Lymphocytes Promote Resolution of CD8-Mediated Lung Injury in a Mouse Model of Lung Rejection

Author

Wu, Qiang, primary, Gardiner, Gail J., additional, Berry, Elizabeth, additional, Wagner, Sarah R., additional, Lu, Tiffany, additional, Clay, Bryan S., additional, Moore, Tamson V., additional, Ferreira, Caroline M., additional, Williams, Jesse W., additional, Luster, Andrew D., additional, Medoff, Benjamin D., additional, Cannon, Judy L., additional, Sperling, Anne I., additional, and Shilling, Rebecca A., additional

Published
2013
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13. Novel Copolymers of Styrene. 2. Oxy Ring-Substituted 2-Cyano-3-phenyl 2-propenamides

Author

Kharas, Gregory B., primary, Hill, Benjamin L., additional, Agos, Christopher H., additional, Bosco, Paula J., additional, Camacho, Jose F., additional, Clay, Bryan S., additional, Clementz, Mia E., additional, Jasionowski, Theodore, additional, Krupka, Rebecca A., additional, Muise, Michael J., additional, Nelson, Elizabeth A., additional, Pavlovsky, Gene, additional, Semp, Melissa C., additional, Sherman, Andrew C., additional, and Stanis, Marianne, additional

Published
2013
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20. CD43 Regulates Th2 Differentiation and Inflammation

Author

Cannon, Judy L., primary, Collins, Amélie, additional, Mody, Purvi D., additional, Balachandran, Diwaker, additional, Henriksen, Kammi J., additional, Smith, Cassandra E., additional, Tong, Jiankun, additional, Clay, Bryan S., additional, Miller, Stephen D., additional, and Sperling, Anne I., additional

Published
2008
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25. Signaling through Fc gamma RIII is required for optimal T helper type (Th)2 responses and Th2-mediated airway inflammation.

Author

Bandukwala HS, Clay BS, Tong J, Mody PD, Cannon JL, Shilling RA, Verbeek JS, Weinstock JV, Solway J, and Sperling AI

Subjects
Animals, Antigen Presentation, Asthma metabolism, Dendritic Cells metabolism, Female, Hypersensitivity metabolism, Inflammation, Interleukin-10 metabolism, Mice, Mice, Inbred BALB C, Signal Transduction, Toll-Like Receptor 4 metabolism, Gene Expression Regulation, Receptors, IgG metabolism, Th2 Cells metabolism
Abstract

Although inhibitory Fc gamma receptors have been demonstrated to promote mucosal tolerance, the role of activating Fc gamma receptors in modulating T helper type (Th)2-dependent inflammatory responses characteristic of asthma and allergies remains unclear. Here, we demonstrate that signaling via activating Fc gamma receptors in conjunction with Toll-like receptor 4 stimulation modulated cytokine production from bone marrow-derived dendritic cells (DCs) and augmented their ability to promote Th2 responses. Ligation of the low affinity receptor Fc gamma RIII was specifically required for the enhanced Th2 responses, as Fc gamma RIII(-/-) DCs failed to augment Th2-mediated airway inflammation in vivo or induce Th2 differentiation in vitro. Further, Fc gamma RIII(-/-) mice had impaired Th2 cytokine production and exhibited reduced airway inflammation, whereas no defect was found in Fc gamma RI(-/-) mice. The augmentation of Th2 immunity was regulated by interleukin 10 production from the DCs but was distinct and independent of the well-established role of Fc gamma RIII in augmenting antigen presentation. Thus, our studies reveal a novel and specific role for Fc gamma RIII signaling in the regulation of Th cell responses and suggest that in addition to immunoglobulin (Ig)E, antigen-specific IgG also contributes to the pathogenesis of Th2-mediated diseases such as asthma and allergies.

Published
2007
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