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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Demethylation of TNFSF7 contributes to CD70 overexpression in CD4+ T cells from patients with systemic sclerosis
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Demethylation of TNFSF7 contributes to CD70 overexpression in CD4+ T cells from patients with systemic sclerosis

机译：TNFSF7的去甲基化导致系统性硬化症患者CD4 + T细胞中CD70过表达

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The pathogenesis of systemic sclerosis (SSc) is still unclear. CD70, a B cell costimulatory molecule that interacts with CD27 during B-T cell contact, is overexpressed due to demethylation of its promoter regulatory elements in CD4+ T cells from patients with the following autoimmune diseases, namely systemic lupus erythematosus (SLE), subacute cutaneous lupus erythematosus (SCLE) and primary Sj?gren's syndrome (pSS). However, as an autoimmune disease, it is unknown whether aberrant expression and methylation of CD70 occur in SSc CD4+ T cells. We aimed to investigate whether the aberrant expression and methylation status of CD70 occur in CD4+ T cells from patients with SSc. We found that the CD70 is overexpressed and the CD70 promoter region is demethylated in SSc CD4+ T cells. These findings suggest that demethylation of CD70 promoter region contributes to the overexpression of CD70 in CD4+ T cells and may contribute to autoimmune response in SSc.
机译：全身性硬化症（SSc）的发病机制仍不清楚。 CD70是一种B细胞共刺激分子，在BT细胞接触期间与CD27相互作用，由于其患有以下自身免疫性疾病（即系统性红斑狼疮（SLE），亚急性皮肤性红斑狼疮）的患者的CD4 + T细胞中其启动子调节元件的去甲基化，因此过表达。 （SCLE）和原发性干燥综合征（pSS）。但是，作为自身免疫性疾病，尚不清楚SSc CD4 + T细胞中是否发生CD70的异常表达和甲基化。我们旨在调查SSc患者CD4 + T细胞中是否发生CD70的异常表达和甲基化状态。我们发现CD70过表达并且CD70启动子区域在SSc CD4 + T细胞中脱甲基。这些发现表明，CD70启动子区域的去甲基化有助于CD70 + CD4 + T细胞中CD70的过表达，并可能有助于SSc中的自身免疫应答。

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