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Caspase-7 deficiency protects from endotoxin-induced lymphocyte apoptosis and improves survival

By Mohamed Lamkanfi, Lilian O. Moreira, Patrudu Makena, Diana C. J. Spierings, Kelli Boyd, Peter J. Murray, Douglas R. Green and Thirumala-Devi Kanneganti


Extensive apoptosis of leukocytes during sepsis and endotoxic shock constitutes an important mechanism linked to the excessive mortality associated with these disorders. Caspase inhibitors confer protection from endotoxin-induced lymphocyte apoptosis and improve survival, but it is not clear which caspases mediate lipopolysaccharide (LPS)–induced lymphocyte apoptosis and mortality. We report here that the apoptotic executioner caspase-7 was activated in the splenocytes of LPS-injected mice, suggesting a role for caspase-7 in lymphocyte apoptosis. Indeed, caspase-7–deficient mice were resistant to LPS-induced lymphocyte apoptosis and were markedly protected from LPS-induced lethality independently of the excessive production of serum cytokines. These results reveal for the first time a nonredundant role for caspase-7 in vivo and identify caspase-7 inhibition as a component of the mechanism by which caspase inhibitors protect from endotoxin-induced mortality

Topics: Immunobiology
Publisher: American Society of Hematology
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Provided by: PubMed Central
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