Ubc13 maintains the suppressive function of regulatory T cells and prevents their conversion into effector-like T cells.
Ubc13 maintains the suppressive function of regulatory T cells and prevents their conversion into effector-like T cells.
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DOI：
10.1038/ni.2267
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发表时间：
2012-05
影响因子：
30.5
通讯作者：
Sun, Shao-Cong
中科院分区：
文献类型：
--
作者：
Chang, Jae-Hoon;Xiao, Yichuan;Hu, Hongbo;Jin, Jin;Yu, Jiayi;Zhou, Xiaofei;Wu, Xuefeng;Johnson, Howard M.;Akira, Shizuo;Pasparakis, Manolis;Cheng, Xuhong;Sun, Shao-Cong
维持免疫稳态需要调节性T（Treg）细胞。在这里，我们表明，Treg特异性消融Ubc 13，赖氨酸63特异性泛素结合酶，引起异常的T细胞活化和自身免疫。虽然Ubc 13缺陷不影响Treg细胞存活或Foxp 3表达，但它损害了Treg细胞的体内抑制功能，并使它们对获得T辅助（TH）1-和TH 17-样效应T细胞表型敏感。Ubc 13的这种功能涉及其下游靶点IκB激酶（IKK）。Ubc 13-IKK信号轴控制表达特异性Treg效应分子，包括白细胞介素10（IL-10）和SOCS 1。总的来说，这些发现表明Ubc 13-IKK信号轴调节维持Treg功能并防止Treg细胞获得炎症表型的分子程序。
Maintenance of immune homeostasis requires regulatory T (Treg) cells. Here we show that Treg-specific ablation of Ubc13, a lysine 63-specific ubiquitin-conjugating enzyme, caused aberrant T cell activation and autoimmunity. Although Ubc13 deficiency did not affect Treg cell survival or Foxp3 expression, it impaired the in vivo suppressive function of Treg cells and rendered them sensitive for acquiring T helper (TH) 1- and TH17-like effector T cell phenotypes. This function of Ubc13 involved its downstream target, IκB kinase (IKK). The Ubc13-IKK signaling axis controlled the expression specific Treg effector molecules, including interleukin 10 (IL-10) and SOCS1. Collectively, these findings suggest that the Ubc13-IKK signaling axis regulates the molecular program that maintains Treg function and prevents Treg cells from acquiring inflammatory phenotypes.
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