Document Detail


The epigenetics of autoimmunity.
MedLine Citation:
PMID:  21278766     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The etiology of autoimmune diseases remains largely unknown. Concordance rates in monozygotic twins are lower than 50% while genome-wide association studies propose numerous significant associations representing only a minority of patients. These lines of evidence strongly support other complementary mechanisms involved in the regulation of genes expression ultimately causing overt autoimmunity. Alterations in the post-translational modification of histones and DNA methylation are the two major epigenetic mechanisms that may potentially cause a breakdown of immune tolerance and the perpetuation of autoimmune diseases. In recent years, several studies both in clinical settings and experimental models proposed that the epigenome may hold the key to a better understanding of autoimmunity initiation and perpetuation. More specifically, data support the impact of epigenetic changes in systemic lupus erythematosus, rheumatoid arthritis, multiple sclerosis and other autoimmune diseases, in some cases based on mechanistical observations. We herein discuss what we currently know and what we expect will come in the next future. Ultimately, epigenetic treatments already being used in oncology may soon prove beneficial also in autoimmune diseases.
Authors:
Francesca Meda; Marco Folci; Andrea Baccarelli; Carlo Selmi
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2011-01-31
Journal Detail:
Title:  Cellular & molecular immunology     Volume:  8     ISSN:  2042-0226     ISO Abbreviation:  Cell. Mol. Immunol.     Publication Date:  2011 May 
Date Detail:
Created Date:  2011-05-03     Completed Date:  2011-09-06     Revised Date:  2013-06-30    
Medline Journal Info:
Nlm Unique ID:  101242872     Medline TA:  Cell Mol Immunol     Country:  China    
Other Details:
Languages:  eng     Pagination:  226-36     Citation Subset:  IM    
Affiliation:
Department of Medicine and Hepatobiliary Immunopathology Unit, IRCCS Istituto Clinico Humanitas, Rozzano, Milan, Italy.
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MeSH Terms
Descriptor/Qualifier:
Animals
Autoimmune Diseases / genetics,  immunology,  metabolism*
Autoimmunity / genetics
DNA Methylation*
Epigenesis, Genetic / immunology*
Gene Expression Regulation / immunology
Histones / immunology*
Humans
Protein Processing, Post-Translational*
Grant Support
ID/Acronym/Agency:
ES000002/ES/NIEHS NIH HHS; P30 ES000002/ES/NIEHS NIH HHS; P30 ES000002-48/ES/NIEHS NIH HHS; R21DK075400/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Histones
Comments/Corrections

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