Journal
NATURE IMMUNOLOGY
Volume 1, Issue 6, Pages 496-501Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/82741
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Funding
- NIGMS NIH HHS [GM44118, GM 55194] Funding Source: Medline
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Sepsis induces lymphocyte apoptosis and prevention of lymphocyte death may improve the chances of surviving this disorder. We compared the efficacy of a selective caspase-3 inhibitor to a polycaspase inhibitor and to caspase-3(-/-) mice. Both inhibitors prevented lymphocyte apoptosis and improved survival. Caspase-3(-/-) mice shared a decreased, but not total, block of apoptosis, The polycaspase inhibitor caused a very substantial decrease in bacteremia. Caspase inhibitors did not benefit RAG-I-/- mice, which had a >tenfold increase in bacteremia compared to controls. Adoptive transfer of T cells that overexpressed the anti-apoptotic protein Bcl-2 increased survival. T cells stimulated with anti-CD3 and anti-CD28 produced increased interleukin 2 and interferon gamma by 6 h. Thus, caspase inhibitors enhance immunity by preventing lymphocyte apoptosis and lymphocytes act rapidly, within 24 h, to control infection.
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