McMahan C J, Fink P J
Department of Immunology, University of Washington School of Medicine, Seattle 98195, USA.
Immunity. 1998 Nov;9(5):637-47. doi: 10.1016/s1074-7613(00)80661-5.
Under most circumstances, allelic exclusion at the T cell receptor (TCR)beta locus is tightly regulated. Here, we describe a system in which TCRbeta allelic exclusion is overcome as a result of V(D)J recombination in peripheral CD4+ T cells. In TCRbeta chain transgenic mice, tolerogen-mediated chronic peripheral selection against cells expressing the transgene leads to surface expression of endogenous TCRbeta chains. Peripheral CD4+ T cells reexpress the recombination activating genes, RAG1 and RAG2, and contain signal end intermediates indicative of ongoing V(D)J recombination. The rescue from deletion of mature T cells expressing newly generated TCRbeta chains suggests that receptor revision plays a role in the maintenance of peripheral T cell tolerance.
在大多数情况下，T细胞受体（TCR）β基因座的等位基因排斥受到严格调控。在此，我们描述了一种系统，其中由于外周CD4⁺ T细胞中的V(D)J重组，TCRβ等位基因排斥被克服。在TCRβ链转基因小鼠中，耐受原介导的针对表达转基因细胞的慢性外周选择导致内源性TCRβ链的表面表达。外周CD4⁺ T细胞重新表达重组激活基因RAG1和RAG2，并含有指示正在进行V(D)J重组的信号末端中间体。从表达新产生的TCRβ链的成熟T细胞缺失中拯救出来表明受体修正在外周T细胞耐受性维持中起作用。
