Hiroaki Hayashi

By Naoko Kumagai, Hiroaki Hayashi, Megumi Maeda, Yoshie Miura, Hidenori Matsuzaki, Suni Lee, Yasumitsu Nishimura, Wataru Fujimoto and Takemi Otsuki

Part of the book: Autoimmune Disorders

By Suni Lee, Hiroaki Hayashi, Megumi Maeda, Hidenori Matsuzaki, Naoko Kumagai-Takei, Ying Chen, Kozo Urakami, Masayasu Kusaka, Yasumitsu Nishimura and Takemi Otsuki

Part of the book: Immune Response Activation

By Suni Lee, Hiroaki Hayashi, Naoko Kumaga-Takei, Hidenori Mastzaki, Kei Yoshitome, Nagisa Sada, Masayasu Kusaka, Kozo Uragami, Yasumitsu Nishimura and Takemi Otsuki

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 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.

Part of the book: Autoantibodies and Cytokines