Please use this identifier to cite or link to this item:
Title: The - 383A>C TNFRI polymorphism is associated with soluble levels and clinical activity in rheumatoid arthritis
Author: Valle, Y.
Padilla-Gutierrez, J.R.
Torres-Carrillo, N.M.
Ledezma-Lozano, I.Y.
Corona-Sanchez, E.G.
Vazquez-Del Mercado, M.
Rangel-Villalobos, H.
Gamez-Nava, J.I.
Gonzalez-Lopez, L.
Munoz-Valle, J.F.
Issue Date: 2010
Abstract: Tumor necrosis factor-? (TNF-?) plays a central role in inflammation, and it has been directly implicated in the pathogenesis of rheumatoid arthritis (RA). TNF-? activity is mediated through TNFRI and TNFRII cell surface receptors, which act as physiological attenuators of TNF-? activity. We recruited 190 RA patients and 190 healthy subjects (HS) in order to associate the - 383A>C TNFRI polymorphism with sTNFRI levels and DAS28 score in RA. In results, sTNFRI levels were higher in RA patients than HS (P = 0.04). The - 383A>C TNFRI polymorphism did not show significant differences in both studied groups. However, in the RA group the sTNFRI levels were significantly elevated (P = 0.004) in A/A genotype carriers. In addition, the A/A genotype carriers had the higher DAS28 score than A/C genotype (P = 0.02). These data suggest that - 383A>C TNFRI polymorphism is not a susceptibility marker in RA, whereas the increased levels of sTNFRI could reflect the clinical activity in RA patients. � Springer-Verlag 2009.
Appears in Collections:Producción científica UdeG

Files in This Item:
There are no files associated with this item.

Items in RIUdeG are protected by copyright, with all rights reserved, unless otherwise indicated.