TY - JOUR
T1 - Environmental factors producing autoimmune dysregulation - Chronic activation of T cells caused by silica exposure
AU - Lee, Suni
AU - Hayashi, Hiroaki
AU - Maeda, Megumi
AU - Chen, Ying
AU - Matsuzaki, Hidenori
AU - Takei-Kumagai, Naoko
AU - Nishimura, Yasumitsu
AU - Fujimoto, Wataru
AU - Otsuki, Takemi
N1 - Funding Information:
The authors thank the former member of the Department of Hygiene, Kawasaki Medical School, Professor Ayako Ueki, Drs. Fuminori Hyodoh and Akiko Tomokuni for their excellent experimental achievements. In addition, the authors thank Ms. Tamayo Hatayama, Shoko Yamamoto, Minako Katoh, Naomi Miyahara, Misao Kuroki, Keiko Kimura, Tomoko Sueishi, Yoshiko Yamashita, Satomi Hatada, Haruko Sakaguchi, and Yumika Isozaki for their technical support. Parts of the experimental results shown in this article were supported by Special Coordination Funds for Promoting Science and Technology ( H18-1-3-3-1 , Comprehensive approach on asbestos-related diseases), KAKENHI grants ( 18390186 , 19659153 and 20390178 ), Kawasaki Medical School Project Grants ( 18-601 , 19-603T , 20-410I , 20-603 , 21-606 and 22-A7 ), a Sumitomo Foundation Grant ( 053027 ), a Yasuda Memorial Foundation Grant ( H18 ), funding from the Takeda Science Foundation ( I-2008 ), and a Young Investigator Activating Grant from the Japanese Society of Hygiene ( H18 ).
PY - 2012/7
Y1 - 2012/7
N2 - Autoimmune disorders are induced by various environmental and occupational substances. Among the most typical factors involving these substances, it is well known that silica exposure causes not only pulmonary fibrosis known as silicosis, but also induces autoimmune diseases such as rheumatoid arthritis known as Caplan's syndrome, systemic sclerosis, systemic lupus erythematosus, and anti-neutrophil cytoplasmic autoantibody (ANCA)-related vasculitis/nephritis. To investigate the immunological effects of silica, a focus on the occurrence of autoimmune dysfunction may clarify these autoimmune diseases and develop effective tools for observing silicosis patients (SIL). In this review, our investigation concerns the autoantibodies found in SIL, alteration of CD95/Fas and related molecules in SIL, case-oriented and in vitro analyses of silica-induced activation of responder and regulatory T cells, and supposed mechanisms of reduction of CD4+25+FoxP3+ regulatory T cells (Treg) in SIL. Further studies are required to investigate Th17 and the interaction with Treg in SIL to understand the cellular and molecular mechanisms of environmental and occupational autoimmune disorders.
AB - Autoimmune disorders are induced by various environmental and occupational substances. Among the most typical factors involving these substances, it is well known that silica exposure causes not only pulmonary fibrosis known as silicosis, but also induces autoimmune diseases such as rheumatoid arthritis known as Caplan's syndrome, systemic sclerosis, systemic lupus erythematosus, and anti-neutrophil cytoplasmic autoantibody (ANCA)-related vasculitis/nephritis. To investigate the immunological effects of silica, a focus on the occurrence of autoimmune dysfunction may clarify these autoimmune diseases and develop effective tools for observing silicosis patients (SIL). In this review, our investigation concerns the autoantibodies found in SIL, alteration of CD95/Fas and related molecules in SIL, case-oriented and in vitro analyses of silica-induced activation of responder and regulatory T cells, and supposed mechanisms of reduction of CD4+25+FoxP3+ regulatory T cells (Treg) in SIL. Further studies are required to investigate Th17 and the interaction with Treg in SIL to understand the cellular and molecular mechanisms of environmental and occupational autoimmune disorders.
KW - Autoimmune
KW - CD95/Fas
KW - Regulatory t cell
KW - Silica
KW - Systemic sclerosis
UR - http://www.scopus.com/inward/record.url?scp=84861195888&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84861195888&partnerID=8YFLogxK
U2 - 10.1016/j.imbio.2011.12.009
DO - 10.1016/j.imbio.2011.12.009
M3 - Review article
C2 - 22226303
AN - SCOPUS:84861195888
VL - 217
SP - 743
EP - 748
JO - Immunobiology
JF - Immunobiology
SN - 0171-2985
IS - 7
ER -