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超抗原驱动的T细胞外周缺失。凋亡发生在失去α/βT细胞受体的细胞中。

Superantigen-driven peripheral deletion of T cells. Apoptosis occurs in cells that have lost the alpha/beta T cell receptor.

作者信息

Huang L, Crispe I N

机构信息

Section of Immunobiology, Yale University Medical School, New Haven, CT 06510.

出版信息

J Immunol. 1993 Aug 15;151(4):1844-51.

PMID:8345186
Abstract

Injection of lymphoid cells expressing minor lymphocyte-stimulating antigen-1 (Mls-1a) induces tolerance to the superantigen, and partial deletion of Mls-1a-reactive T cells. We have identified a transient population of T cells that have lost the alpha/beta T cell receptor at the time when Mls-1a-reactive T cells start to disappear during the process of tolerance induction. Apoptosis was directly demonstrated in this TCR-alpha/beta negative T-cell population. This indicates a peripheral T-cell deletion pathway, characterized by TCR down-regulation, apoptosis, and clonal deletion. The consequence of Mls-1a-induced TCR down-regulation appears to be different in CD4+ cells and in CD8+ cells. Although most of the CD4+ cells that have lost TCR expressing alpha- and beta-chains appear to be undergoing apoptosis, many of their CD8+ counterparts may be able to re-express the Ag receptor. This argues for the involvement of coreceptors in the induction of apoptosis during peripheral deletion.

摘要

注射表达次要淋巴细胞刺激抗原-1(Mls-1a)的淋巴细胞可诱导对该超抗原的耐受性,并使Mls-1a反应性T细胞部分缺失。我们已经鉴定出一群短暂存在的T细胞,在耐受性诱导过程中,当Mls-1a反应性T细胞开始消失时,它们已经失去了α/β T细胞受体。在这个TCR-α/β阴性T细胞群体中直接证实了细胞凋亡。这表明存在一种外周T细胞缺失途径,其特征为TCR下调、细胞凋亡和克隆性缺失。Mls-1a诱导的TCR下调在CD4+细胞和CD8+细胞中的后果似乎有所不同。虽然大多数失去表达α链和β链TCR的CD4+细胞似乎正在经历凋亡,但其许多CD8+对应细胞可能能够重新表达抗原受体。这表明共受体参与了外周缺失过程中细胞凋亡的诱导。

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