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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Series: | Mediators of Inflammation |
Online Access: | http://dx.doi.org/10.1155/2017/2608605 |
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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 |
work_keys_str_mv |
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1725632473489997824 |