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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Ig gene-like molecule CD31 plays a nonredundant role in the regulation of T-cell immunity and tolerance
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Ig gene-like molecule CD31 plays a nonredundant role in the regulation of T-cell immunity and tolerance

机译：Ig基因样分子CD31在调节T细胞免疫和耐受中起非冗余作用

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CD31 is an Ig-like molecule expressed by leukocytes and endothelial cells with an established role in the regulation of leukocyte trafficking. Despite genetic deletion of CD31 being associated with exacerbation of T cell-mediated autoimmunity, the contribution of this molecule to T-cell responses is largely unknown. Here we report that tumor and allograft rejection are significantly enhanced in CD31-def icient mice, which are also resistant to tolerance induction. We propose that these effects are dependent on an as yet unrecognized role for CD31-mediated homophilic interactions between T cells' and antigen-presenting cells (APCs) during priming. We show that loss of CD31 interactions leads to enhanced primary clonal expansion, increased killing capacity, and diminished regulatory functions by T cells. Immunomodulation by CD31 signals correlates with a partial inhibition of proximal T-cell receptor (TCR) signaling, specifically Zap-70 phosphorylation. However, CD31-deficient mice do not develop autoimmunity due to increased T-cell death following activation, and we show that CD31 triggering induces Erk-mediated prosurvival activity in T cells either in conjunction with TCR signaling or autonomously. We conclude that CD31 functions as a nonredundant comodulator of T-cell responses, which specializes in sizing the ensuing immune response by setting the threshold for T-cell activation and tolerance, while preventing memory T-cell death.
机译：CD31是由白细胞和内皮细胞表达的Ig样分子，在白细胞运输的调节中具有确定的作用。尽管CD31的遗传缺失与T细胞介导的自身免疫的加剧有关，但该分子对T细胞反应的贡献在很大程度上尚不清楚。在这里，我们报告肿瘤和同种异体排斥反应在CD31缺陷小鼠中显着增强，这些小鼠也对耐受诱导具有抗性。我们建议这些影响取决于在启动过程中T细胞和抗原呈递细胞（APC）之间CD31介导的同质相互作用的尚未认识的作用。我们表明，CD31相互作用的丧失会导致增强的主要克隆扩展，增加的杀伤能力，并减少T细胞的调节功能。 CD31信号的免疫调节与部分抑制近端T细胞受体（TCR）信号有关，特别是Zap-70磷酸化。但是，缺乏CD31的小鼠由于激活后T细胞死亡的增加而不会产生自身免疫，并且我们证明CD31触发结合TCR信号传导或自主诱导Erk介导的T细胞存活活性。我们得出的结论是，CD31充当T细胞反应的非冗余协同调节因子，它专门通过设定T细胞活化和耐受性的阈值来确定随后的免疫反应的大小，同时防止记忆性T细胞死亡。

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