Molecular Pathogenesis Program, Kimmel Center for Biology and Medicine at the Skirball Institute, Department of Pathology, New York University School of Medicine, New York, New York, USA.
J Clin Invest. 2010 Dec;120(12):4190-2. doi: 10.1172/JCI45262. Epub 2010 Nov 22.
Deleterious immune responses that cause autoimmune diseases such as type 1 diabetes are normally kept in check by a myriad of mechanisms. Among these, protection mediated by CD4+Foxp3+ Tregs constitutes an essential pathway. Much work over the past decade aimed to understand how Tregs affect immune responses triggered by effector T cells (Teffs), but less is known about how Teffs affect Tregs. In this issue of the JCI, Grinberg-Bleyer et al. report the clearest example thus far regarding this important aspect of Treg biology. They find that in mice, sustained protection from diabetes by Tregs is dependent on Teffs and partially dependent on TNF-α, a cytokine traditionally considered proinflammatory.
导致 1 型糖尿病等自身免疫性疾病的有害免疫反应通常受到多种机制的控制。在这些机制中，CD4+Foxp3+Tregs 介导的保护构成了一个重要途径。在过去的十年中，大量的工作旨在了解 Tregs 如何影响效应 T 细胞（Teffs）引发的免疫反应，但对于 Teffs 如何影响 Tregs 知之甚少。在本期 JCI 中，Grinberg-Bleyer 等人报道了迄今为止关于 Treg 生物学这一重要方面的最清晰示例。他们发现，在小鼠中，Tregs 对糖尿病的持续保护依赖于 Teffs，部分依赖于 TNF-α，一种传统上被认为具有促炎作用的细胞因子。
