Environmental factors producing autoimmune dysregulation - Chronic activation of T cells caused by silica exposure

Suni Lee, Hiroaki Hayashi, Megumi Maeda, Ying Chen, Hidenori Matsuzaki, Naoko Takei-Kumagai, Yasumitsu Nishimura, Wataru Fujimoto, Takemi Otsuki

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)743-748
Number of pages6
JournalImmunobiology
Volume217
Issue number7
DOIs
Publication statusPublished - Jul 2012

Fingerprint

Silicosis
Silicon Dioxide
T-Lymphocytes
Regulatory T-Lymphocytes
Autoantibodies
Autoimmune Diseases
Caplan Syndrome
Nephritis
Pulmonary Fibrosis
Systemic Scleroderma
Vasculitis
Systemic Lupus Erythematosus
Rheumatoid Arthritis
Neutrophils

Keywords

  • Autoimmune
  • CD95/Fas
  • Regulatory t cell
  • Silica
  • Systemic sclerosis

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Hematology

Cite this

Environmental factors producing autoimmune dysregulation - Chronic activation of T cells caused by silica exposure. / Lee, Suni; Hayashi, Hiroaki; Maeda, Megumi; Chen, Ying; Matsuzaki, Hidenori; Takei-Kumagai, Naoko; Nishimura, Yasumitsu; Fujimoto, Wataru; Otsuki, Takemi.

In: Immunobiology, Vol. 217, No. 7, 07.2012, p. 743-748.

Research output: Contribution to journalArticle

Lee, S, Hayashi, H, Maeda, M, Chen, Y, Matsuzaki, H, Takei-Kumagai, N, Nishimura, Y, Fujimoto, W & Otsuki, T 2012, 'Environmental factors producing autoimmune dysregulation - Chronic activation of T cells caused by silica exposure', Immunobiology, vol. 217, no. 7, pp. 743-748. https://doi.org/10.1016/j.imbio.2011.12.009
Lee, Suni ; Hayashi, Hiroaki ; Maeda, Megumi ; Chen, Ying ; Matsuzaki, Hidenori ; Takei-Kumagai, Naoko ; Nishimura, Yasumitsu ; Fujimoto, Wataru ; Otsuki, Takemi. / Environmental factors producing autoimmune dysregulation - Chronic activation of T cells caused by silica exposure. In: Immunobiology. 2012 ; Vol. 217, No. 7. pp. 743-748.
@article{f931e26305d14d8fac312f59acca51c9,
title = "Environmental factors producing autoimmune dysregulation - Chronic activation of T cells caused by silica exposure",
abstract = "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.",
keywords = "Autoimmune, CD95/Fas, Regulatory t cell, Silica, Systemic sclerosis",
author = "Suni Lee and Hiroaki Hayashi and Megumi Maeda and Ying Chen and Hidenori Matsuzaki and Naoko Takei-Kumagai and Yasumitsu Nishimura and Wataru Fujimoto and Takemi Otsuki",
year = "2012",
month = "7",
doi = "10.1016/j.imbio.2011.12.009",
language = "English",
volume = "217",
pages = "743--748",
journal = "Immunobiology",
issn = "0171-2985",
publisher = "Urban und Fischer Verlag GmbH und Co. KG",
number = "7",

}

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

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 - Article

C2 - 22226303

AN - SCOPUS:84861195888

VL - 217

SP - 743

EP - 748

JO - Immunobiology

JF - Immunobiology

SN - 0171-2985

IS - 7

ER -