Department of Dermatology, Second Xiangya Hospital, Central South University, 139 Ren-Min Road, Changsha 410011, China.
Clin Immunol. 2012 Apr;143(1):39-44. doi: 10.1016/j.clim.2012.01.005. Epub 2012 Jan 18.
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 Sjögren'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.
系统性硬化症（SSc）的发病机制尚不清楚。CD70 是一种 B 细胞共刺激分子，在 B-T 细胞接触过程中与 CD27 相互作用，由于其启动子调节元件的去甲基化，在患有以下自身免疫性疾病的患者的 CD4+T 细胞中过度表达，即系统性红斑狼疮（SLE）、亚急性皮肤型红斑狼疮（SCLE）和原发性干燥综合征（pSS）。然而，作为一种自身免疫性疾病，CD70 的异常表达和甲基化是否发生在 SSc CD4+T 细胞中尚不清楚。我们旨在研究 SSc CD4+T 细胞中是否存在 CD70 的异常表达和甲基化状态。我们发现，CD70 在 SSc CD4+T 细胞中过度表达，且 CD70 启动子区域去甲基化。这些发现表明 CD70 启动子区域的去甲基化导致 CD70 在 CD4+T 细胞中的过度表达，并可能导致 SSc 中的自身免疫反应。
