FAS(CD95) FASL INTERACTIONS REQUIRED FOR PROGRAMMED CELL-DEATH AFTER T-CELL ACTIVATION
FAS(CD95) FASL INTERACTIONS REQUIRED FOR PROGRAMMED CELL-DEATH AFTER T-CELL ACTIVATION
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DOI：
10.1038/373444a0
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发表时间：
1995-02-02
期刊：
影响因子：
64.8
通讯作者：
MARSHAKROTHSTEIN, A
中科院分区：
文献类型：
--
作者：
JU, ST;PANKA, DJ;MARSHAKROTHSTEIN, A
T细胞杂交瘤的受体交联诱导细胞活化，随后细胞凋亡（1-6）。这种激活诱导的细胞死亡需要重新合成RNA和蛋白质（1-3），但提供死亡信号的实际基因产物尚未鉴定（4-6）。我们在这里表明，受体交联诱导Fas配体和上调Fas，并随后参与Fas的Fas配体激活细胞死亡程序。可溶性Fas-免疫球蛋白融合蛋白可选择性阻止细胞死亡，但不能阻止细胞活化。因此，Fas和Fas配体是死亡基因的产物，它们之间的相互作用解释了活化诱导T细胞死亡的分子机制。
RECEPTOR crosslinking of T-cell hybridomas induces cell activation followed by apoptosis(1-6). This activation-induced cell death requires de novo synthesis of RNA and proteins(1-3), but the actual gene products that provide the death signal have not been identified(4-6). We show here that receptor crosslinking induces Fas ligand and upregulates Fas, and that the ensuing engagement of Fas by Fas ligand activates the cell-death programme. Cell death, but not activation, can be selectively prevented by a soluble Fas-immunoglobulin fusion protein. Thus, Fas and Fas ligand are the death-gene products, and their interaction accounts for the molecular mechanism of activation-induced T-cell death.