Masteller Emma L, Tang Qizhi, Bluestone Jeffrey A
UCSF Diabetes Center, Department of Medicine, University of California, 513 Parnassus Avenue, HSW 1118, Box 0540, San Francisco, CA 94143-0540, USA.
Semin Immunol. 2006 Apr;18(2):103-10. doi: 10.1016/j.smim.2006.01.004. Epub 2006 Feb 3.
CD4(+)CD25(+)Foxp3(+) regulatory T cells (Treg) are critical for the regulation of tolerance and have shown enormous potential in suppressing pathological immune responses in autoimmune disease, transplantation, and graft-versus-host disease (GVHD). Recent data indicate that suppression of organ-specific autoimmunity is critically dependent on the antigen specificity of the Treg. An emerging model of Treg action is that organ-specific Treg acquire suppressive activity through activation by dendritic cells expressing organ-derived antigens. Thus, efficacy of Treg-based therapy should be increased by using organ-specific Treg rather than polyclonal Treg. This necessitates the ability to identify relevant antigens and to expand rare antigen-specific Treg from diverse polyclonal populations. Here, we consider the importance of antigen specificity in Treg function and discuss recent advances for the expansion of antigen-specific Treg and the therapeutic potential of Treg in controlling autoimmunity and GVHD.
CD4(+)CD25(+)Foxp3(+)调节性T细胞（Treg）对于耐受性调节至关重要，并且在抑制自身免疫性疾病、移植和移植物抗宿主病（GVHD）中的病理性免疫反应方面显示出巨大潜力。最近的数据表明，器官特异性自身免疫的抑制严重依赖于Treg的抗原特异性。一种新兴的Treg作用模型是，器官特异性Treg通过表达器官衍生抗原的树突状细胞激活而获得抑制活性。因此，使用器官特异性Treg而非多克隆Treg应可提高基于Treg的治疗效果。这就需要具备识别相关抗原以及从不同多克隆群体中扩增稀有抗原特异性Treg的能力。在此，我们探讨抗原特异性在Treg功能中的重要性，并讨论抗原特异性Treg扩增的最新进展以及Treg在控制自身免疫和GVHD方面的治疗潜力。
