Ex-TFRs: A Missing Piece of the SLE Puzzle?

Ex-TFRs: A Missing Piece of the SLE Puzzle?
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前 TFR:SLE 拼图中缺失的一块?

DOI:
10.3389/fimmu.2021.662305
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发表时间:
2021
影响因子:
7.3
通讯作者:
Zhou X
Zhou X
中科院分区:
医学2区
文献类型:
--
作者:
Wei X;Zhang J;Zhou X

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系统性红斑狼疮(SLE)是一种慢性多器官自身免疫性疾病,涉及广泛的自身抗体的产生和补体激活。这些高亲和力自身抗体的产生需要T细胞/B细胞协作以及生发中心(GC)的形成。T滤泡调节细胞(TFR)是功能性特化T调节细胞(TCRs),其保护自身反应性T细胞和B细胞。然而,最近的证据表明,TFR并不总是稳定的,并且可以失去Foxp 3表达而成为获得有效效应子功能的致病性“ex-TFR”。在这篇综述中,我们总结了有关TFR稳定性调节的内在和外在机制的文献,并讨论了TFR重编程在自身抗体产生和SLE发病机制中的潜在作用。
Systemic lupus erythematosus (SLE) is a chronic multi-organ autoimmune disease involving the production of a wide range of autoantibodies and complement activation. The production of these high-affinity autoantibodies requires T cell/B cell collaboration as well as germinal center (GC) formation. T follicular regulatory cells (TFRs) are functional specialized T regulatory cells (Tregs) that safeguard against both self-reactive T and B cells. However, recent evidence suggests that TFRs are not always stable and can lose Foxp3 expression to become pathogenic “ex-TFRs” that gain potent effector functions. In this review, we summarize the literature on intrinsic and extrinsic mechanisms of regulation of TFR stability and discuss the potential role of TFR reprogramming in autoantibody production and SLE pathogenesis.
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发表时间: 2019-10-01
期刊: NATURE IMMUNOLOGY
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