Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Science. 2023 Nov 3;382(6670):534-541. doi: 10.1126/science.adh4124. Epub 2023 Nov 2.
CD8 T cell tolerance is thought to result from clonal deletion of autoreactive thymocytes before they differentiate into mature CD8 T cells in the thymus. However, we report that, in mice, CD8 T cell tolerance instead results from premature thymic eviction of immature autoreactive CD8 thymocytes into the periphery, where they differentiate into self-tolerant mature CD8 T cells. Premature thymic eviction is triggered by T cell receptor (TCR)-driven down-regulation of the transcriptional repressor Gfi1, which induces expression of sphingosine-1-phosphate receptor-1 (S1P1) on negatively selected immature CD8 thymocytes. Thus, premature thymic eviction is the basis for CD8 T cell tolerance and is the mechanism responsible for the appearance in the periphery of mature CD8 T cells bearing autoreactive TCRs that are absent from the thymus.
CD8 T 细胞耐受被认为是由于自身反应性胸腺细胞在胸腺中分化为成熟 CD8 T 细胞之前发生克隆性缺失所致。然而,我们报告称,在小鼠中,CD8 T 细胞耐受反而源自不成熟的自身反应性 CD8 胸腺细胞过早地从胸腺中逐出到外周,在那里它们分化为自身耐受的成熟 CD8 T 细胞。过早的胸腺逐出是由 T 细胞受体(TCR)驱动的转录抑制因子 Gfi1 的下调触发的,该下调诱导负选择的不成熟 CD8 胸腺细胞表达鞘氨醇-1-磷酸受体-1(S1P1)。因此,过早的胸腺逐出是 CD8 T 细胞耐受的基础,也是导致外周成熟 CD8 T 细胞出现的机制,这些细胞带有自身反应性 TCR,但在胸腺中不存在。