A central role for induced regulatory T cells in tolerance induction in experimental colitis.
A central role for induced regulatory T cells in tolerance induction in experimental colitis.
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DOI：
10.4049/jimmunol.0802535
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发表时间：
2009-03-15
期刊：
影响因子：
--
通讯作者：
Williams CB
中科院分区：
文献类型：
--
作者：
Haribhai D;Lin W;Edwards B;Ziegelbauer J;Salzman NH;Carlson MR;Li SH;Simpson PM;Chatila TA;Williams CB
除了胸腺衍生的或天然的T调节（nTreg）细胞之外，诱导的T调节（iTreg）细胞的第二子集从外周中的常规CD4+ T细胞从头产生。在结肠炎的CD45RB高CD4 + T细胞转移模型中检查了iTreg细胞在耐受性中的功能。原位生成的iTreg细胞在体外抑制T细胞增殖的能力方面与nTreg细胞相似，并且它们在体内的缺乏加速了肠道疾病。用nTreg细胞治疗解决了结肠炎，但仅当iTreg细胞也存在时。尽管iTreg细胞需要Foxp3来获得抑制活性和表型稳定性，但它们的基因表达谱与已建立的nTreg“基因签名”不同，这表明发育差异和可能的机制差异。这些结果鉴定了iTreg细胞在体内的功能性作用，并证明iTreg和nTreg细胞两者可协同作用以维持耐受性。
In addition to thymus-derived or natural T regulatory (nTreg) cells, a second subset of induced T regulatory (iTreg) cells arises de novo from conventional CD4+ T cells in the periphery. The function of iTreg cells in tolerance was examined in a CD45RBhighCD4+ T cell transfer model of colitis. In situ-generated iTreg cells were similar to nTreg cells in their capacity to suppress T cell proliferation in vitro and their absence in vivo accelerated bowel disease. Treatment with nTreg cells resolved the colitis, but only when iTreg cells were also present. Although iTreg cells required Foxp3 for suppressive activity and phenotypic stability, their gene expression profile was distinct from the established nTreg “genetic signature,” indicative of developmental and possibly mechanistic differences. These results identified a functional role for iTreg cells in vivo and demonstrated that both iTreg and nTreg cells can act in concert to maintain tolerance.
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