Autoantibodies in Silicosis Patients: Silica-Induced Dysregulation of Autoimmunity

Suni Lee, H. Hayashi, Naoko Kumaga-Takei, Hidenori Mastzaki, K. Yoshitome, N. Sada, M. Kusaka, K. Uragami, Y. Nishimura, T. Otsuki
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引用次数: 3

Abstract

Silica particles cause silicosis (SIL) and represent one of the most typical environmental and occupational substances that induce autoimmune disorders among the exposed popu-lation. Anti-nuclear antibody (ANA), anti-Sjögren’s-syndrome-related antigen A (SS-A), anti-centromere protein B (CENP)-B, and anti-scleroderma (Scl)-70 autoantibodies were examined in SIL and compared with those in healthy volunteers (HV) and patients with systemic sclerosis (SSc). Individuals with SIL were prone to autoimmune diseases and some autoantibodies seemed to be important as an estimation of this condition. Anti-Fas autoan- tibody found in SIL was functionally capable of inducing apoptosis in Fas-expressing cells, and this may cause a decrease of regulatory T cells (Tregs) expressing Fas in SIL. Moreover, responder T cells (Tresps) in SIL seemed to be activated chronically and protected from Fas-mediated apoptosis. Thus, an imbalance of Tresps (dominant) and Tregs (less) occurred in SIL. All of these causes of SIL are ready to further develop autoimmune diseases.
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矽肺患者的自身抗体:二氧化硅诱导的自身免疫失调
二氧化硅颗粒引起矽肺病(SIL),是暴露人群中诱发自身免疫性疾病的最典型的环境和职业物质之一。检测SIL患者的抗核抗体(ANA)、anti-Sjögren综合征相关抗原A (SS-A)、抗着丝粒蛋白B (CENP)-B和抗硬皮病(Scl)-70自身抗体,并与健康志愿者(HV)和系统性硬化症(SSc)患者进行比较。SIL患者易患自身免疫性疾病,一些自身抗体似乎是评估这种疾病的重要指标。在SIL中发现的抗Fas自身抗体在功能上能够诱导表达Fas的细胞凋亡,这可能导致SIL中表达Fas的调节性T细胞(Tregs)减少。此外,SIL中的应答T细胞(Tresps)似乎是慢性激活的,并保护其免受fas介导的凋亡。因此,在SIL中出现了Tresps(显性)和Tregs(较少)的不平衡。所有这些SIL的病因都有可能进一步发展为自身免疫性疾病。
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