Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto, Japan.
Nat Immunol. 2010 Jan;11(1):7-13. doi: 10.1038/ni.1818. Epub 2009 Dec 17.
Immunological self tolerance is maintained at least in part by regulatory T (T(reg)) cells that actively and dominantly control potentially hazardous self-reactive T cells in the periphery. Antigens that stimulate self-reactive T cells may also activate natural T(reg) cells, thereby maintaining dominant self tolerance. Conversely, genetic anomalies or environmental agents that specifically or predominantly affect T(reg) cells cause or predispose to autoimmunity. With recent advances in our understanding of T(reg) cell development in the thymus and periphery and the molecular mechanism of T(reg) cell-mediated suppression, new ways of treating immunological diseases by targeting T(reg) cells at the cellular and molecular levels are envisaged.
免疫自我耐受至少部分是由调节性 T（Treg）细胞维持的，这些细胞在外周主动且优势地控制潜在危险的自身反应性 T 细胞。刺激自身反应性 T 细胞的抗原也可能激活天然 Treg 细胞，从而维持优势的自身耐受。相反，特异性或主要影响 Treg 细胞的遗传异常或环境因素导致或易患自身免疫。随着我们对 Treg 细胞在胸腺和外周中的发育以及 Treg 细胞介导的抑制的分子机制的理解的最新进展，通过在细胞和分子水平上针对 Treg 细胞来治疗免疫性疾病的新方法已经可以预见。
