English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/47586
logo share SHARE logo core CORE   Add this article to your Mendeley library MendeleyBASE

Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL | DATACITE
Exportar a otros formatos:


Antibodies against β-fibrin synthetic peptides: A study of their association with the immunogenetic background and disease course of rheumatoid arthritis patients

AuthorsHaro Villar, Isabel ; Gómara Elena, María José ; Pérez Rodríguez, María L.; Viñas, Odette; Ercilla, Guadalupe; Gómez-Puerta, José A.; Sanmartí, Raimon
Rheumatoid arthritis
Shared epitope
Issue Date2011
CitationEuropean Journal of Medicinal Chemistry
AbstractPreliminary studies have shown the potential application for the diagnosis of Rheumatoid Arthritis (RA) patients with a severe disease course of an epitopic domain of β-fibrin. The aim of the present work was the analysis of the presence of antibodies against several β-fibrin synthetic peptides in relation to the immunogenetic background and disease course in a clinically well-defined RA patient cohort. Our results indicated that positive patients against anti-β-fibrin synthetic peptides have a higher percentage of HLA-DRB1 shared epitope (SE) than negative patients. We also observed that the presence of SE alleles was significantly associated with a higher level of anti-[Cit376]βfib(365–383) antibodies. When analyzing the effect of different SE alleles, we found a significant positive association between carriers of QRRAA allele and [Cit376]βfib(365–383) (Odds ratio 3.77; CI95%: 1.41–10.08). These results suggest that the anti-β-fibrin status is associated with the immunogenetic background of RA patients.
Publisher version (URL)http://dx.doi.org/10.1016/j.ejmech.2011.01.024
Appears in Collections:(IQAC) Artículos
Files in This Item:
There are no files associated with this item.
Show full item record
Review this work

Related articles:

WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.