The role of FOXP3 in autoimmunity

被引：27
|
作者：
Pesenacker, Anne M. [1 ,2 ]
Cook, Laura [1 ,2 ]
Levings, Megan K. [1 ,2 ]
机构：
[1] Univ British Columbia, Dept Surg, Vancouver, BC V5Z 1M9, Canada
[2] BC Childrens Hosp, Res Inst, Vancouver, BC, Canada
来源：
CURRENT OPINION IN IMMUNOLOGY | 2016年 / 43卷
关键词：
REGULATORY T-CELLS; TRANSCRIPTION FACTOR FOXP3; DEMETHYLATED REGION; PROTEIN; GENE; DISEASES; THERAPY; PHOSPHORYLATION; MECHANISMS; EXPRESSION;
D O I：
10.1016/j.coi.2016.07.004
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
FOXP3 controls the development and function of T regulatory cells (Tregs). Autoimmunity is linked to changes in FOXP3 activity that can occur at multiple levels and lead to Treg dysfunction. For example, changes in IL-2 signaling, FOXP3 transcription and/or post-translational modifications can all contribute to loss of self-tolerance. As additional pathways of FOXP3 regulation are elucidated, new therapeutic approaches to increase Treg activity either by cell therapy or pharmacological intervention are being tested. Early success from pioneering studies of Treg-based therapy in transplantation has promoted the undertaking of similar studies in autoimmunity, with emerging evidence for the effectiveness of these approaches, particularly in the context of type 1 diabetes.
引用
收藏
页码：16 / 23
页数：8
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