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T cell hybridomasのAICDはFas誘導性細胞死と同様のプロテアーゼカスケードを有するが Dexamethasoneによる細胞死とは異なる：山下眞一¹、池井　聰¹、水谷純一¹、土井口幸¹、芳賀克夫¹,　荒井光広¹、鶴本泰之¹、Pierre Vassalli²、小川道雄³（¹国立熊本病院・外、²ジュネーブ大学・病理、³熊本大.　二外.）

Activation-induced cell death (AICD) in the T cell hybridomas use the similar proteases activation cascade as Fas-mediated cell death, but different from Dexamethasone-induced cell death : Shin-ichi YAMASHITA1, Satoshi IKEI1, Jun-ichi MIZUTANI1, Miyuki DOIGUCHI1, Yoshio HAGA1, Mitsuhiro ARAI1, Yasuyuki TSURUMOTO1, Pierre Vassalli2, Michio OGAWA (1 Dept. of Surg., National Kumamoto Hosp., 2Dept. of Path., Univ. de Geneve,　3 Dept. of Surg., Kumamoto Univ. )

Activation-induced cell death(AICD) in T cell hybridomas is a model of negative selection in immature T cell. This pathway is closely related to Fas-FasL interaction and antagonized by glucocorticoid. We here demonstrate that anti-CD3 cross-linking sequentially leads to activation of cysteine proteases of the interleukin-1b converting enzyme(ICE) and CPP32 types in T cell hybridomas as similar protease activation cascade as Fas-mediated cell death, and dexamethasone activates CPP32 like-proteases without ICE like-proteases activation. Although activation of T cell hybridomas induce G1/S block followed by apoptosis, anti-Fas cross-linking is not related to cell cycle. These observation are consistent with p21 induction in AICD and suggest that the early stage of AICD is different from Fas-mediated cell death . Taken together, these three types of cell death is closely related each other , and regulated in Tcell development.