Department of Pediatrics, and the Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Curr Mol Med. 2012 Dec;12(10):1261-72. doi: 10.2174/156652412803833634.
Type 1 diabetes mellitus (T1DM) is a T cell-mediated autoimmune disease resulting in islet β cell destruction, hypoinsulinemia, and severely altered glucose homeostasis. T1DM has classically been attributed to the pathogenic actions of auto-reactive effector T cells(Teffs) on the β cell. Recent literature now suggests that a failure of a second T cell subtype, known as regulatory T cells (Tregs), plays a critical role in the development of T1DM. During immune homeostasis, Tregs counterbalance the actions of autoreactive Teff cells, thereby participating in peripheral tolerance. An imbalance in the activity between Teff and Tregs may be crucial in the breakdown of peripheral tolerance, leading to the development of T1DM. In this review, we summarize our current understanding of Treg function in health and in T1DM, and examine the effect of experimental therapies for T1DM on Treg cell number and function in both mice and humans.
1 型糖尿病（T1DM）是一种 T 细胞介导的自身免疫性疾病，导致胰岛β细胞破坏、胰岛素分泌不足和严重改变的葡萄糖稳态。T1DM 经典地归因于自身反应性效应 T 细胞（Teffs）对β细胞的致病作用。最近的文献表明，第二种 T 细胞亚型，即调节性 T 细胞（Tregs）的功能障碍在 T1DM 的发展中起着关键作用。在免疫稳态中，Tregs 抵消了自身反应性 Teff 细胞的作用，从而参与外周耐受。Teff 和 Tregs 之间活性的不平衡可能在打破外周耐受中至关重要，导致 T1DM 的发展。在这篇综述中，我们总结了我们目前对 Treg 在健康和 T1DM 中的功能的理解，并研究了 T1DM 的实验治疗对小鼠和人类 Treg 细胞数量和功能的影响。
