The Histone Modification Code in the Pathogenesis of Autoimmune Diseases

Autoimmune diseases are chronic inflammatory disorders caused by a loss of self-tolerance, which is characterized by the appearance of autoantibodies and/or autoreactive lymphocytes and the impaired suppressive function of regulatory T cells. The pathogenesis of autoimmune diseases is extremely comp...

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Main Authors: Yasuto Araki, Toshihide Mimura
Format: Article
Language:English
Published: Hindawi Limited 2017-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2017/2608605
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spelling doaj-b2b9c49d1d134d1f95c8a55959d882f22020-11-24T23:03:43ZengHindawi LimitedMediators of Inflammation0962-93511466-18612017-01-01201710.1155/2017/26086052608605The Histone Modification Code in the Pathogenesis of Autoimmune DiseasesYasuto Araki0Toshihide Mimura1Department of Rheumatology and Applied Immunology, Faculty of Medicine, Saitama Medical University, Saitama, JapanDepartment of Rheumatology and Applied Immunology, Faculty of Medicine, Saitama Medical University, Saitama, JapanAutoimmune diseases are chronic inflammatory disorders caused by a loss of self-tolerance, which is characterized by the appearance of autoantibodies and/or autoreactive lymphocytes and the impaired suppressive function of regulatory T cells. The pathogenesis of autoimmune diseases is extremely complex and remains largely unknown. Recent advances indicate that environmental factors trigger autoimmune diseases in genetically predisposed individuals. In addition, accumulating results have indicated a potential role of epigenetic mechanisms, such as histone modifications, in the development of autoimmune diseases. Histone modifications regulate the chromatin states and gene transcription without any change in the DNA sequence, possibly resulting in phenotype alteration in several different cell types. In this paper, we discuss the significant roles of histone modifications involved in the pathogenesis of autoimmune diseases, including rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, primary biliary cirrhosis, and type 1 diabetes.http://dx.doi.org/10.1155/2017/2608605
collection DOAJ
language English
format Article
sources DOAJ
author Yasuto Araki
Toshihide Mimura
spellingShingle Yasuto Araki
Toshihide Mimura
The Histone Modification Code in the Pathogenesis of Autoimmune Diseases
Mediators of Inflammation
author_facet Yasuto Araki
Toshihide Mimura
author_sort Yasuto Araki
title The Histone Modification Code in the Pathogenesis of Autoimmune Diseases
title_short The Histone Modification Code in the Pathogenesis of Autoimmune Diseases
title_full The Histone Modification Code in the Pathogenesis of Autoimmune Diseases
title_fullStr The Histone Modification Code in the Pathogenesis of Autoimmune Diseases
title_full_unstemmed The Histone Modification Code in the Pathogenesis of Autoimmune Diseases
title_sort histone modification code in the pathogenesis of autoimmune diseases
publisher Hindawi Limited
series Mediators of Inflammation
issn 0962-9351
1466-1861
publishDate 2017-01-01
description Autoimmune diseases are chronic inflammatory disorders caused by a loss of self-tolerance, which is characterized by the appearance of autoantibodies and/or autoreactive lymphocytes and the impaired suppressive function of regulatory T cells. The pathogenesis of autoimmune diseases is extremely complex and remains largely unknown. Recent advances indicate that environmental factors trigger autoimmune diseases in genetically predisposed individuals. In addition, accumulating results have indicated a potential role of epigenetic mechanisms, such as histone modifications, in the development of autoimmune diseases. Histone modifications regulate the chromatin states and gene transcription without any change in the DNA sequence, possibly resulting in phenotype alteration in several different cell types. In this paper, we discuss the significant roles of histone modifications involved in the pathogenesis of autoimmune diseases, including rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, primary biliary cirrhosis, and type 1 diabetes.
url http://dx.doi.org/10.1155/2017/2608605
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