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特发性炎性肌病中的 FOXP3+ T 调节细胞。

FOXP3+ T regulatory cells in idiopathic inflammatory myopathies.

机构信息

Department of Neurology, Julius-Maximilians-University, Wuerzburg, Germany.

出版信息

J Neuroimmunol. 2010 Aug 25;225(1-2):137-42. doi: 10.1016/j.jneuroim.2010.03.013.

DOI:10.1016/j.jneuroim.2010.03.013
PMID:20537411
Abstract

FOXP3+ T regulatory cells (Tregs) are considered key players in the maintenance of immune homeostasis. Here we studied the presence and potential role of FOXP3+ Tregs in myositis. CD3 and FOXP3 expression in dermatomyositis, polymyositis and inclusion body myositis was assessed by immunohistochemistry and real-time PCR. FOXP3+ Tregs were found in close proximity to effector cells and their numbers correlated with the degree of inflammation. Despite divergent pathogenetic concepts, we observed no differences in the frequency of FOXP3 immunoreactive cells or FOXP3 mRNA expression between different myositis entities. Functional assays using human myoblasts as targets of CD8+ cells demonstrate that Tregs are capable to inhibit the lytic activity of cytotoxic cells. Our data suggest that FOXP3 Tregs serve to counterbalance muscle destruction by cytotoxic T cells in myositis.

摘要

叉头框蛋白 P3+调节性 T 细胞(Tregs)被认为是维持免疫稳态的关键因素。在这里,我们研究了 FOXP3+Tregs 在肌炎中的存在及其潜在作用。通过免疫组织化学和实时 PCR 评估了皮肌炎、多发性肌炎和包涵体肌炎中 CD3 和 FOXP3 的表达。FOXP3+Tregs 与效应细胞紧密相邻,其数量与炎症程度相关。尽管发病机制概念不同,但我们在不同肌炎实体中观察到 FOXP3 免疫反应性细胞的频率或 FOXP3 mRNA 表达无差异。使用人类成肌细胞作为 CD8+细胞的靶标进行的功能测定表明,Tregs 能够抑制细胞毒性细胞的溶细胞活性。我们的数据表明,FOXP3+Tregs 可通过细胞毒性 T 细胞来抵消肌炎中的肌肉破坏。

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