Zheng Song Guo
Division of Rheumatology and Immunology, Department of Medicine, University of Southern California, Keck School of Medicine Los Angeles, CA 90033, USA.
Int J Clin Exp Med. 2008;1(3):192-202. Epub 2008 Jun 10.
Foxp3+T regulatory cell (Treg) subsets play a crucial role in the maintenance of immune homeostasis against self-antigen. The lack or dysfunction of these cells is responsible for the pathogenesis and development of many autoimmune diseases. Therefore, manipulation of these cells may provide a novel therapeutic approach to treat autoimmune diseases and prevent allograft rejection during organ transplantation. In the article, we will provide current opinions concerning the classification, developmental and functional characterizations of Treg subsets. A particular emphasis will be focused on transforming cell growth factor beta (TGF-beta) and its role in the differentiation and development of induced regulatory T cells (iTregs) in the periphery. Moreover, the similarity and disparity of iTregs and naturally occurring, thymus-derived CD4+CD25+Foxp3+ regulatory T cells (nTregs) will also be discussed. While proinflammatory cytokine IL-6 can convert nTregs to IL-17-producing cells, peripheral Tregs induced by TGF-beta are resistant to this cytokine. This difference may affect the role of each in the adaptive immune response.
Foxp3+调节性T细胞（Treg）亚群在维持针对自身抗原的免疫稳态中发挥着关键作用。这些细胞的缺乏或功能障碍是许多自身免疫性疾病发病机制和发展的原因。因此，对这些细胞的调控可能为治疗自身免疫性疾病和预防器官移植期间的同种异体移植排斥提供一种新的治疗方法。在本文中，我们将提供有关Treg亚群分类、发育和功能特征的当前观点。将特别强调转化生长因子β（TGF-β）及其在外周诱导调节性T细胞（iTreg）分化和发育中的作用。此外，还将讨论iTreg与天然存在的、胸腺来源的CD4+CD25+Foxp3+调节性T细胞（nTreg）的异同。虽然促炎细胞因子IL-6可将nTreg转化为产生IL-17的细胞，但由TGF-β诱导的外周Treg对这种细胞因子具有抗性。这种差异可能会影响它们各自在适应性免疫反应中的作用。
