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Exposure of naive murine CD4 + T lymphocytes to superantigen such as staphylococcal enterotoxin B (SEB) induces a strong proliferative response. Prolonged exposure or subsequent restimulation of the responding T cell population with SEB leads to the apoptotic events of activation-induced cell death (AICD). The signaling mechanism responsible for the AICD is a target of intensive investigation. However, the precise downstream signaling pathways of SEB-induced AICD remains unclear. Our results here show that the sequential activation of caspase-1/ICE-like and caspase-3/CPP32-like cysteine proteases probably plays a role in the signaling transduction of SEB-induced AICD, but caspase-3/CPP32-like proteases activation does not depend on caspase-1-like proteases activation. Herbimycin A, a specific inhibitor of protein tyrosine kinases, inhibit caspase-3/CPP32-like cysteine proteases activation. However, it does not prevent DNA fragmentation of CD4 + T cells apoptosis induced by SEB. These results indicate that protein tyrosine kinases pathway is probably involved in the signaling transduction of CD4 + T cells apoptosis induced by SEB and “crosstalks” with the pathway of caspase-3/CPP32-like proteases activation.
Exposure of naive murine CD4 + T lymphocytes to superantigen such as staphylococcal enterotoxin B (SEB) induces a strong proliferative response. Prolonged exposure or subsequent restimulation of the responding T cell population with SEB leads to the apoptotic events of activation-induced cell death (AICD The results show that the sequential activation of caspase-1 / ICE-like and caspase- 3 / CPP32-like cysteine proteases probably plays a role in the signaling transduction of SEB-induced AICD, but caspase-3 / CPP32-like proteases activation does not depend on caspase-1-like proteases activation. Herbimycin A, a specific inhibitor of However, it does not prevent DNA fragmentation of CD4 + T cells induced by SEB. These results indicate that protein tyrosine kinases pathway is probably involved in the signaling transduction of CD4 + T cells apoptosis induced by SEB and “crosstalks” with the pathway of caspase-3 / CPP32-like proteases activation.