Epigenetics of Autoantigens: New Opportunities for Therapy of Autoimmune Diseases
The field of epigenetics requires that traditional divisions between scientific disciplines give way to cross-fertilization of concepts and ideas from different areas of investigation. Such is the case with research in autoimmunity. Recent discoveries of stimuli that induce autoimmunity reveal that...
Main Authors: | , |
---|---|
Format: | Article |
Language: | English |
Published: |
SAGE Publishing
2013-01-01
|
Series: | Genetics and Epigenetics |
Online Access: | https://doi.org/10.4137/GEG.S12144 |
id |
doaj-4a0c115f8a554469a651b4f81e0b5bf0 |
---|---|
record_format |
Article |
spelling |
doaj-4a0c115f8a554469a651b4f81e0b5bf02020-11-25T01:03:10ZengSAGE PublishingGenetics and Epigenetics1179-237X2013-01-01510.4137/GEG.S12144Epigenetics of Autoantigens: New Opportunities for Therapy of Autoimmune DiseasesMarko Radic0Sylviane Muller1Department of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, USA.Immunopathology and therapeutic chemistry/Laboratory of excellence MEDALIS, Institut de Biologie Molέculaire et Cellulaire, CNRS, Strasbourg, France.The field of epigenetics requires that traditional divisions between scientific disciplines give way to cross-fertilization of concepts and ideas from different areas of investigation. Such is the case with research in autoimmunity. Recent discoveries of stimuli that induce autoimmunity reveal that epigenetic marks of autoantigens are recognized by autoreactive B and T cell receptors. Thus, insights into the initiation of autoimmunity, its prevention and therapy will arise from understanding the biochemistry, cell biology and microbiology of autoantigen epigenetics. Here, we highlight potential benefits from the inhibition of a histone modifying enzyme and the administration of a phosphorylated, spliceosome-derived peptide, in the treatment of autoimmunity.https://doi.org/10.4137/GEG.S12144 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Marko Radic Sylviane Muller |
spellingShingle |
Marko Radic Sylviane Muller Epigenetics of Autoantigens: New Opportunities for Therapy of Autoimmune Diseases Genetics and Epigenetics |
author_facet |
Marko Radic Sylviane Muller |
author_sort |
Marko Radic |
title |
Epigenetics of Autoantigens: New Opportunities for Therapy of Autoimmune Diseases |
title_short |
Epigenetics of Autoantigens: New Opportunities for Therapy of Autoimmune Diseases |
title_full |
Epigenetics of Autoantigens: New Opportunities for Therapy of Autoimmune Diseases |
title_fullStr |
Epigenetics of Autoantigens: New Opportunities for Therapy of Autoimmune Diseases |
title_full_unstemmed |
Epigenetics of Autoantigens: New Opportunities for Therapy of Autoimmune Diseases |
title_sort |
epigenetics of autoantigens: new opportunities for therapy of autoimmune diseases |
publisher |
SAGE Publishing |
series |
Genetics and Epigenetics |
issn |
1179-237X |
publishDate |
2013-01-01 |
description |
The field of epigenetics requires that traditional divisions between scientific disciplines give way to cross-fertilization of concepts and ideas from different areas of investigation. Such is the case with research in autoimmunity. Recent discoveries of stimuli that induce autoimmunity reveal that epigenetic marks of autoantigens are recognized by autoreactive B and T cell receptors. Thus, insights into the initiation of autoimmunity, its prevention and therapy will arise from understanding the biochemistry, cell biology and microbiology of autoantigen epigenetics. Here, we highlight potential benefits from the inhibition of a histone modifying enzyme and the administration of a phosphorylated, spliceosome-derived peptide, in the treatment of autoimmunity. |
url |
https://doi.org/10.4137/GEG.S12144 |
work_keys_str_mv |
AT markoradic epigeneticsofautoantigensnewopportunitiesfortherapyofautoimmunediseases AT sylvianemuller epigeneticsofautoantigensnewopportunitiesfortherapyofautoimmunediseases |
_version_ |
1725202086149226496 |