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首页> 外文期刊>Nature >Activation of human CD4~+ cells with CD3 and CD46 induces a T-regulatory cell 1 phenotype
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Activation of human CD4~+ cells with CD3 and CD46 induces a T-regulatory cell 1 phenotype

机译：用CD3和CD46激活人CD4〜+细胞诱导T调节细胞1表型

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摘要

The immune system must distinguish not only between self and non-self, but also between innocuous and pathological foreign antigens to prevent unnecessary or self-destructive immune responses. Unresponsiveness to harmless antigens is established through central and peripheral processes. Whereas clonal deletion and anergy are mechanisms of peripheral tolerance, active suppression by T-regulatory 1 (Tr1) cells has emerged as an essential factor in the control of autoreactive cells. Trl cells are CD4~+ T lymphocytes that are defined by their production of interleukin 10 (IL-10) and suppression of T-helper cells; however, the physiological conditions underlying Trl differentiation are unknown. Here we show that co-engagement of CD3 and the complement regulator CD46 in the presence of IL-2 induces a Tr1-specific cytokine phenotype in human CD4~+ T cells. These CD3/CD46-stimulated IL-10-producing CD4~+ cells proliferate strongly, suppress activation of bystander T cells and acquire a memory phenotype. Our findings identify an endogenous receptor-mediated event that drives Trl differentiation and suggest that the complement system has a previously unappreciated role in T-cell-mediated immunity and tolerance.
机译：免疫系统不仅必须区分自身和非自身，还必须区分无害和病理性外源抗原，以防止不必要的或自我破坏的免疫反应。对无害抗原的无反应性是通过中央和周围过程建立的。克隆缺失和无反应是外周耐受的机制，而T调节1（Tr1）细胞的主动抑制已成为控制自身反应性细胞的重要因素。 Trl细胞是CD4〜+ T淋巴细胞，由其产生白介素10（IL-10）和抑制T辅助细胞来定义；然而，Tr1分化的潜在生理条件尚不清楚。在这里，我们显示在IL-2存在下CD3和补体调节剂CD46的共同参与在人CD4 + T细胞中诱导Tr1特异性细胞因子表型。这些CD3 / CD46刺激的产生IL-10的CD4 +细胞强烈增殖，抑制旁观者T细胞的激活并获得记忆表型。我们的发现确定了驱动Trl分化的内源性受体介导的事件，并表明补体系统在T细胞介导的免疫和耐受中具有以前未被认识的作用。

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