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首页> 外文期刊>Annual Review of Immunology >FOXP3: of mice and men.
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FOXP3: of mice and men.

机译：FOXP3：老鼠和男人。

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The immune system has evolved mechanisms to recognize and eliminate threats, as well as to protect against self-destruction. Tolerance to self-antigens is generated through two fundamental mechanisms: (a) elimination of self-reactive cells in the thymus during selection and (b) generation of a variety of peripheral regulatory cells to control self-reactive cells that escape the thymus. It is becoming increasing apparent that a population of thymically derived CD4+ regulatory T cells, exemplified by the expression of the IL-2Ralpha chain, is essential for the maintenance of peripheral tolerance. Recent work has shown that the forkhead family transcription factor Foxp3 is critically important for the development and function of the regulatory T cells. Lack of Foxp3 leads to development of fatal autoimmune lymphoproliferative disease; furthermore, ectopic Foxp3 expression can phenotypically convert effector T cells to regulatory T cells. This review focuses on Foxp3 expression and function and highlights differences between humans and mice regarding Foxp3 regulation.
机译：免疫系统已经进化出识别和消除威胁以及防止自我毁灭的机制。对自身抗原的耐受是通过两种基本机制产生的：（a）在选择过程中消除胸腺中的自反应性细胞;（b）产生各种外周调节细胞以控制逃避胸腺的自反应性细胞。越来越明显的是，以胸腺来源的CD4 +调节性T细胞群体（以IL-2Ralpha链的表达为例）对于维持外周耐受至关重要。最近的工作表明，叉头家族转录因子Foxp3对于调节性T细胞的发育和功能至关重要。 Foxp3缺乏导致致命的自身免疫性淋巴组织增生性疾病的发展;此外，异位Foxp3表达可以将效应T细胞表型转化为调节性T细胞。这篇综述着重于Foxp3的表达和功能，并强调了人类和小鼠在Foxp3调控方面的差异。

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