UNIMPAIRED THYMIC AND PERIPHERAL T-CELL DEATH IN MICE LACKING THE NUCLEAR RECEPTOR NGFI-B (NUR77)
UNIMPAIRED THYMIC AND PERIPHERAL T-CELL DEATH IN MICE LACKING THE NUCLEAR RECEPTOR NGFI-B (NUR77)
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DOI：
10.1126/science.7624775
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发表时间：
1995-07-28
期刊：
影响因子：
56.9
通讯作者：
MILBRANDT, J
中科院分区：
文献类型：
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作者：
LEE, SL;WESSELSCHMIDT, RL;MILBRANDT, J
T细胞杂交瘤需要立即早期基因NGFI-B（nur 77）用于T细胞受体（TCR）介导的凋亡，这是一种用于自身反应性T细胞的阴性选择的模型。在携带NGFI-B功能丧失突变的小鼠中检查TCR介导的死亡，通过给予CD 3抗体（抗CD 3）或在两种表达自身反应性TCR的充分表征的转基因模型中进行。胸腺细胞死亡的程度和速率均未受损。抗CD 3诱导的死亡在CD 4+外周T细胞中是正常的，其中死亡主要由Fas信号通路介导。因此，没有观察到胸腺或外周T细胞死亡对NGFI-B的独特需求。
T cell hybridomas require the immediate-early gene NGFI-B (nur77) for T cell receptor (TCR)-mediated apoptosis, a model for negative selection of self-reactive T cells. TCR-mediated death was examined in mice bearing an NGFI-B loss-of-function mutation, either by administration of antibodies to CD3 (anti-CD3) or in two well-characterized transgenic models expressing self-reactive TCRs. Both the extent and the rate of thymocyte death were unimpaired. Anti-CD3-induced death was normal in CD4+ peripheral T cells, in which death is mediated predominantly by the Fas signaling pathway. Thus, no unique requirement for NGFI-B is observed for thymic or peripheral T cell death.