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TRAF6 directs commitment to regulatory T cells in thymocytes

机译：TRAF6指导对胸腺细胞中调节性T细胞的承诺

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摘要

Regulatory T cells (Tregs), a subset of CD4+ helper T cells, are crucial for immunological self-tolerance. Defect in development or function of Tregs results in autoimmune disease in human and mice. Whereas it is known that Tregs mainly develop in the thymus, the molecular mechanism underlying development of Treg is not fully understood. TRAF6-deficient mice showed a severe defect in the Treg development in thymus. In vitro fetal thymic organ culture experiments indicated that the defect is ascribed to the absence of TRAF6 in thymic cells. Moreover, mixed fetal liver transfer experiments revealed that the development of Foxp3+ cells differentiated from Traf6-/- hematopoietic cells was specifically impaired in the thymus, indicating cell-intrinsic requirement for TRAF6 in the Treg development. On the other hand, TRAF6 is not required for the development of conventional CD4+ T cell. In addition, TGF beta-dependent induction of Foxp3 in CD4+ T cells in vitro was not impaired by the absence of TRAF6. Overall, our data indicate that TRAF6 plays an essential role on the commitment of immature thymocytes to thymic Tregs in cell-intrinsic fashion.
机译：调节性T细胞（Tregs）是CD4 +辅助性T细胞的一个子集，对免疫学自我耐受性至关重要。 Tregs发育或功能缺陷会导致人类和小鼠自身免疫性疾病。尽管已知Tregs主要在胸腺中发育，但尚未完全了解Treg发育的分子机制。缺乏TRAF6的小鼠在胸腺的Treg发育中显示严重缺陷。体外胎儿胸腺器官培养实验表明，该缺陷归因于胸腺细胞中不存在TRAF6。此外，混合的胎儿肝脏转移实验表明，从Traf6-/-造血细胞分化而来的Foxp3 +细胞的发育在胸腺中受到了特别的损害，表明Treg发育中TRAF6的细胞内在需求。另一方面，传统的CD4 + T细胞的开发不需要TRAF6。此外，TRAF6的存在不会损害体外CD4 + T细胞中TGFβ依赖性Foxp3的诱导。总的来说，我们的数据表明，TRAF6在未成熟胸腺细胞对胸腺Treg的承诺中起着至关重要的作用。

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