Document Detail


Innate immunity, epigenetics and autoimmunity in rheumatoid arthritis.
MedLine Citation:
PMID:  19232437     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease characterized by the progressive and irreversible destruction of joints. RA remains an incurable condition, although a new class of drugs, biologicals, have made a major breakthrough in targeting and/or eliminating the immune cells, including T cells, B cells and monocytes/macrophages from the joints. That we cannot (yet?) cure the disease is most likely due to the lack of therapeutic targeting the endogenously activated RA synovial fibroblasts (RASF). Most interestingly, RASF express Toll-like receptors (TLRs) 1-6 rendering them prone to activation by exogenous and endogenous TLR ligands and resulting in the production of numerous powerful chemokines and cytokines. These factors are responsible for the repopulation of immune cells in the joints after ceasing cell depleting therapies. To characterize the molecular mechanisms of synovial activation, a new approach studying the epigenetic characteristics of RASF has been recently undertaken. Thereby, the pattern of histone acetylation, DNA methylation and gene expression regulating microRNA are being explored. Since auto-antibodies have the most predictive and diagnostic value for RA, it is challenging to study more comprehensively the contribution of auto-antibodies to the disease. A new screening technique, serological analysis of recombinant human cDNA expression library (SEREX), adapted from cancer research allowed for the identification of novel auto-antibodies in RA, including anti-serpin E2 auto-antibodies. The serpin E2 auto-antibodies were found to inhibit the activity of serpin E2 and have potentially a functional role in the disease. The recent findings in the field of innate immunity, epigenetics and autoimmunity related to the pathogenesis of RA are in the scope of this review.
Authors:
Hanna Maciejewska Rodrigues; Astrid J??ngel; Renate E Gay; Steffen Gay
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-02-15
Journal Detail:
Title:  Molecular immunology     Volume:  47     ISSN:  1872-9142     ISO Abbreviation:  Mol. Immunol.     Publication Date:  2009 Nov 
Date Detail:
Created Date:  2009-11-03     Completed Date:  2010-01-25     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7905289     Medline TA:  Mol Immunol     Country:  England    
Other Details:
Languages:  eng     Pagination:  12-8     Citation Subset:  IM    
Affiliation:
Center of Experimental Rheumatology, University Hospital Zurich/Zurich Center for Integrative Human Physiology (ZIHP), University of Zurich, Gloriastrasse 23-25, CH-8091 Zurich, Switzerland. hanna.maciejewska@usz.ch
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MeSH Terms
Descriptor/Qualifier:
Animals
Arthritis, Rheumatoid / etiology,  genetics,  immunology*
Autoantibodies
Autoimmunity*
Epigenesis, Genetic / immunology*
Humans
Immunity, Innate*
Chemical
Reg. No./Substance:
0/Autoantibodies

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