Chun Shiang Chung

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Apoptosis of CD4(+) T cells and T(H)2 polarization are hallmarks of sepsis-induced immunoparalysis. In this study, we characterized sepsis-induced adaptive immune dysfunction and examined whether improving T-cell effector function can improve outcome to sepsis. We found that septic mice produced less antigen-specific T-cell-dependent IgM and IgG(2a)(More)
A proper innate inflammatory response is essential for prevention of the systemic inflammation associated with sepsis. BTLA is an immune-regulatory receptor demonstrated to be expressed not only on adaptive immune populations and have potent inhibitory effects on CD4(+) T cells but is also expressed on innate cell populations (CD11c(+) and CD11b(+) cells)(More)
BACKGROUND The etiology of sepsis is broad. The peritoneal cavity displays compartmentalization with respect to inflammatory responses, so peripheral blood responses to sepsis of abdominal vs. non-abdominal origin are expected to be divergent. Lymphocytes and invariant natural killer T (iNKT) cells play important roles in survival from sepsis, as they(More)
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