| First Author | Lamkanfi M | Year | 2009 |
| Journal | Blood | Volume | 113 |
| Issue | 12 | Pages | 2742-5 |
| PubMed ID | 19168786 | Mgi Jnum | J:146876 |
| Mgi Id | MGI:3838704 | Doi | 10.1182/blood-2008-09-178038 |
| Citation | Lamkanfi M, et al. (2009) Caspase-7 deficiency protects from endotoxin-induced lymphocyte apoptosis and improves survival. Blood 113(12):2742-5 |
| abstractText | 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. |
