Mechanisms of exTreg induction.
Mechanisms of exTreg induction.
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DOI:
10.1002/eji.202049123
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发表时间:
2021-08
影响因子:
5.4
通讯作者:
Bromberg JS
中科院分区:
文献类型:
--
作者:
Saxena V;Lakhan R;Iyyathurai J;Bromberg JS
CD4+CD25+Foxp3+ regulatory T cells (Tregs) play an important role in the maintenance of the immune system by regulating immune responses and resolving inflammation. Tregs exert their function by suppressing other immune cells and mediating peripheral self-tolerance. Under homeostatic conditions, Tregs are stable T cell populations. However, under inflammatory environments, Tregs are converted to CD4+CD25lowFoxp3low cells. These cells are termed “exTreg” or “exFoxp3” cells. The molecular mechanism of Treg transition to exTregs remains incompletely understood. Uncertainties might be explained by a lack of consensus of biological markers to define Treg subsets in general and exTregs in particular. In this review, we summarize known markers of Tregs and factors responsible for exTreg generation including cytokines, signaling pathways, transcription factors, and epigenetic mechanisms. We also identify studies demonstrating the presence of exTregs in various diseases and sources of exTregs. Understanding the biology of Treg transition to exTregs will help in designing Treg-based therapeutic approaches. The plasticity of regulatory T cells (Tregs) is required for their function of immune suppression. During homeostasis, Treg stability is maintained by an interplay of several factors. Inflammation induced perturbations affect Treg stability resulting in their conversion to exTregs/exFoxp3. We provide a mechanistic overview of exTreg generation.
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