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10 results on '"Fay, Katherine T."'

4. Junctional adhesion molecule-A deletion increases phagocytosis and improves survival in a murine model of sepsis

Author

Klingensmith, Nathan J., primary, Fay, Katherine T., additional, Swift, David A., additional, Bazzano, Julia M.R., additional, Lyons, John D., additional, Chen, Ching-wen, additional, Meng, Mei, additional, Ramonell, Kimberly M., additional, Liang, Zhe, additional, Burd, Eileen M., additional, Parkos, Charles A., additional, Ford, Mandy L., additional, and Coopersmith, Craig M., additional

Published
2022
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5. Increased mortality in CD43-deficient mice during sepsis

Author

Fay, Katherine T., primary, Chihade, Deena B., additional, Chen, Ching-Wen, additional, Klingensmith, Nathan J., additional, Lyons, John D., additional, Ramonell, Kimberly, additional, Liang, Zhe, additional, Coopersmith, Craig M., additional, and Ford, Mandy L., additional

Published
2018
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10. CXCR4 blockade decreases CD4+ T cell exhaustion and improves survival in a murine model of polymicrobial sepsis.

Author

Ramonell, Kimberly M., Zhang, Wenxiao, Hadley, Annette, Chen, Ching-wen, Fay, Katherine T., Lyons, John D., Klingensmith, Nathan J., McConnell, Kevin W., Coopersmith, Craig M., and Ford, Mandy L.

Subjects
CHEMOKINE receptors, SEPTICEMIA treatment, T cells, CD4 antigen, MULTIPLE organ failure, ANTI-inflammatory agents, ANIMAL models in research
Abstract

Sepsis is a dysregulated systemic response to infection involving many inflammatory pathways and the induction of counter-regulatory anti-inflammatory processes that results in a state of immune incompetence and can lead to multi-organ failure. CXCR4 is a chemokine receptor that, following ligation by CXCL12, directs cells to bone marrow niches and also plays an important role in T cell cosignaling and formation of the immunological synapse. Here, we investigated the expression and function of CXCR4 in a murine model of polymicrobial sepsis. Results indicate that CXCR4 is selectively upregulated on naïve CD4+ and CD8+ T cells and CD4+ central memory T cells following the induction of sepsis, and that CXCR4 antagonism resulted in a significant decrease in sepsis-induced mortality. We probed the mechanistic basis for these findings and found that CXCR4 antagonism significantly increased the number of peripheral CD4+ and CD8+ T cells following sepsis. Moreover, mice treated with the CXCR4 antagonist contained fewer PD-1+ LAG-3+ 2B4+ cells, suggesting that blockade of CXCR4 mitigates CD4+ T cell exhaustion during sepsis. Taken together, these results characterize CXCR4 as an important pathway that modulates immune dysfunction and mortality following sepsis, which may hold promise as a target for future therapeutic intervention in septic patients. [ABSTRACT FROM AUTHOR]

Published
2017
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