**Autoantibodies in Silicosis Patients: Silica-Induced Dysregulation of Autoimmunity Dysregulation of Autoimmunity**

**Autoantibodies in Silicosis Patients: Silica-Induced** 

DOI: 10.5772/intechopen.72999

Suni Lee, Hiroaki Hayashi, Naoko Kumaga-Takei, Hidenori Mastzaki, Kei Yoshitome, Nagisa Sada, Masayasu Kusaka, Kozo Uragami, Yasumitsu Nishimura and Takemi Otsuki Hidenori Mastzaki, Kei Yoshitome, Nagisa Sada, Masayasu Kusaka, Kozo Uragami, Yasumitsu Nishimura and Takemi Otsuki Additional information is available at the end of the chapter

Suni Lee, Hiroaki Hayashi, Naoko Kumaga-Takei,

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/intechopen.72999

#### **Abstract**

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Epub 2013 Dec 29

134 Autoantibodies and Cytokines

2005;**64**:1244-1245

2017;**8**(18):30039-30049

Silica particles cause silicosis (SIL) and represent one of the most typical environmental and occupational substances that induce autoimmune disorders among the exposed population. 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 autoantibody 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 Fasmediated 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.

**Keywords:** silicosis, anti-CENP-B autoantibody, anti-Fas autoantibody, apoptosis, regulatory T cell, responder T cell
