The study was aimed to analyze expression of nuclear factor of activated T cells (NFATs ), forkhead box P3 (FOXP3), and their associated genes (sCTLA4, flCTLA4, IL10, TGFB, IL2, IL4, CD25) in regulatory T cells (Tregs) of 48 generalized vitiligo (GV) patients and 45 unaffected controls. The transcripts of NFATC1 to NFATC4, FOXP3, IL10, flCTLA4 (p  < .0001), NFAT5 (p  = .0003), sCTLA4 (p  = .001), and FOXP3 protein in Tregs and plasma IL‐10 levels were reduced significantly (p  < .0001) in GV Tregs compared to controls. The FOXP3 promoter polymorphisms [rs3761548(C > A), rs3761547(A > G), and rs2232365(A > G)] revealed significantly decreased FOXP3 protein levels in patients' Tregs with susceptible AA, GG, and GG genotypes (p  < .0001, p  = .028, p  = .022, respectively). The active vitiligo Tregs showed reduced levels of NFATC3, NFATC4 , NFAT5, FOXP3, TGFB, and flCTLA4 transcripts (p  = .0005, p  = .0003, p  = .0002, p  = .020, p  < .0001, p  = .006, respectively) and FOXP3 and TGF‐β proteins (p  = .0394 and p  = .0013) compared to stable vitiligo. Early‐onset patients (1–20 years) demonstrated decreased IL‐10, sCTLA‐4, flCTLA‐4, TGFB, and FOXP3 transcripts and FOXP3 protein as compared to late‐onset patients (41–60 years) (p  = .001, p  = .003, p  = .009, p  = .005, p  = .038, p  = .0226, respectively). Overall, our results for the first time suggest a likely role of NFATs and FOXP3 together with Treg immune‐suppressive genes in GV pathogenesis and disease progression, warranting additional investigations.

中文翻译：

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广泛性白癜风患者调节性T细胞中活化T细胞，叉头盒P3和免疫抑制基因的核因子表达改变。

该研究旨在分析活化T细胞（NFATs），叉头盒P3（FOXP3）及其相关基因（CTLA4，flCTLA4，IL10，TGFB，IL2，IL4，CD25）的核因子在调节性T细胞（ 48位广义白癜风（GV）患者和45位未受影响的对照的Tregs。的转录NFATC1到NFATC4，FOXP3，IL10，flCTLA4（p  <0.0001），NFAT5（p  = 0.0003），sCTLA4（p  = 0.001），和FOXP3蛋白在调节性T细胞和血浆IL10水平降低显著（ 与对照相比，GV Treg中的p <.0001）。该FOXP3启动子多态性[rs3761548（C> A），rs3761547（A> G）和rs2232365（A> G）]显示，患有易感性AA，GG和GG基因型的患者Treg中FOXP3蛋白水平显着降低（p  <.0001，p  = .028，p  = .022）。活性的Treg白癜风显示出降低的水平NFATC3，NFATC4，NFAT5，FOXP3，TGFB，和flCTLA4转录物（p  = 0.0005，p  = 0.0003，p  = 0.0002，p  = 0.020，p  <0.0001，p  =。 006）和FOXP3和TGF-β蛋白（p  = .0394和p = .0013）与稳定的白癜风相比。与迟发型患者（41-60岁）相比，早发型患者（1-20岁）表现出IL-10，sCTLA-4，flCTLA-4，TGFB和FOXP3转录本和FOXP3蛋白的降低（p  = .001 ，p  = 0.003，p  = 0.009，p  = 0.005，p  = 0.038，p  = 0.0226，分别地）。总体而言，我们的结果首次表明NFAT和FOXP3以及Treg免疫抑制基因可能在GV发病机制和疾病进展中发挥作用，值得进一步研究。