Linkage between PTK Signaling Pathway “Crosstalking” and Caspase-3／ CPP32-1ike Proteases Activation in Signaling Transduction of CD4^＋ T Lymphocytes Apoptosis Induced by Superantigen SEB-中国期刊网

摘要 ExposureofnaivemurineCD4^+TlymphocytestosuperantigensuchasstaphylococcalenterotoxinB(SEB)inducesastrongproliferativeresponse.ProlongedexposureorsubsequentrestimulationoftherespondingTcellpopulationwithSEBleadstotheapoptoticeventsofactivation-inducedcelldeath(AICD).ThesignalingmechanismresponsiblefortheAICDisatargetofintensiveinvestigation.However,theprecisedownstreamsignahngpathwaysofSEB-inducedAICDremainsunclear.Ourresultshereshowthatthesequentialactivationofcaspase-1/ICE-hkeandcaspase-3/CPP32-hkecysteineproteasesprobablyplaysaroleinthesignalingtransductionofSEB-inducedAICD,butcaspase-3/CPP32-hkeproteasesactivationdoesnotdependoncaspase-1-likeproteasesactivation.HerbimycinA,aspecificinhibitorofproteintyresinekinases,inhibitcaspase-3/CPP32-1ikecysteineproteasesactivation.However,itdoesnotpreventDNAfragmentationofCD4^+TcellsapoptosisinducedbySEB.TheseresultsindicatethatproteintyrosinekinasespathwayisprobablyinvolvedinthesignalingtransductionofCD4^+TcellsapoptosisinducedbySEBand“crosstalks”withthepathwayofcaspase-3/CPP32-1ikeproteasesactivation.

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Linkage between PTK Signaling Pathway “Crosstalking” and Caspase-3／ CPP32-1ike Proteases Activation in Signaling Transduction of CD4^＋ T Lymphocytes Apoptosis Induced by Superantigen SEB

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Linkage between PTK Signaling Pathway “Crosstalking” and Caspase-3／ CPP32-1ike Proteases Activation in Signaling Transduction of CD4^＋ T Lymphocytes Apoptosis Induced by Superantigen SEB

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