Allelic inclusion of T cell receptor α genes poses an autoimmune hazard due to low-level expression of autospecific receptors
Allelic inclusion of T cell receptor α genes poses an autoimmune hazard due to low-level expression of autospecific receptors
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DOI：
10.1016/s1074-7613(00)80561-0
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发表时间：
1998-05-01
期刊：
影响因子：
32.4
通讯作者：
von Boehmer, H
中科院分区：
文献类型：
--
作者：
Sarukhan, A;Garcia, C;von Boehmer, H
器官特异性自身免疫性疾病可由逃避自身耐受诱导的α β T细胞引起。在这里，我们表明逃避自身耐受的原因之一是同一细胞共表达两种不同的T细胞受体，这可能发生在正常小鼠中高达30%的所有T细胞中，并可能导致自身特异性TCR的低水平表面表达。我们发现，双受体表达T细胞可以逃避耐受性，即使是普遍表达的抗原，但仍然可以诱导自身免疫性糖尿病时，相关蛋白在胰腺组织中表达。然而，在表达自身特异性TCR作为唯一受体的T细胞中不存在这种致糖尿病性T细胞。
Organ-specific autoimmune disease can be caused by alpha beta T cells that have escaped self-tolerance induction. Here we show that one of the causes of escape from self-tolerance is the coexpression of two different T cell receptors by the same cell, which can occur in up to 30% of all T cells in normal mice and can lead to low-level surface expression of an autospecific TCR. We found that double receptor-expressing T cells can escape tolerance even to ubiquitously expressed antigens but can nevertheless induce autoimmune diabetes when the relevant protein is expressed in pancreatic tissue. Such diabetogenic T cells are absent, however, among T cells expressing the autospecific TCR as the sole receptor.