期刊
JOURNAL OF IMMUNOLOGY
卷 197, 期 10, 页码 3762-3770出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1601118
关键词
-
类别
资金
- National Institutes of Health [R01 DK089125, P01 AI108545, T32 AI089443]
Regulatory T cells (Tregs) are critical regulators of peripheral immune tolerance. Treg insufficiency can lead to autoimmune disorders, including type 1 diabetes (T1D). Increasing evidence in mouse models of T1D, as well as other autoimmune disorders, suggests that there are defects in Treg-mediated suppression. Indeed, whereas Treg frequency in the peripheral blood of T1D patients is unaltered, their suppressive abilities are diminished compared with Tregs in healthy controls. Although expression of the transcription factor Foxp3 is a prerequisite for Treg development and function, there are many additional factors that can alter their stability, survival, and function. Much has been learned in other model systems, such as tumors, about the mechanism and pathways that control Treg stability and function. This review poses the question of whether we can use these findings to develop new therapeutic approaches that might boost Treg stability, survival, and/or function in T1D and possibly other autoimmune disorders.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据