Published in:
01-03-2010 | Original Article
The −383A>C TNFRI polymorphism is associated with soluble levels and clinical activity in rheumatoid arthritis
Authors:
Y. Valle, J. R. Padilla-Gutiérrez, N. M. Torres-Carrillo, I. Y. Ledezma-Lozano, E. G. Corona-Sánchez, M. Vázquez-Del Mercado, H. Rangel-Villalobos, J. I. Gámez-Nava, L. González-López, José Francisco Muñoz-Valle
Published in:
Rheumatology International
|
Issue 5/2010
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Abstract
Tumor necrosis factor-α (TNF-α) plays a central role in inflammation, and it has been directly implicated in the pathogenesis of rheumatoid arthritis (RA). TNF-α activity is mediated through TNFRI and TNFRII cell surface receptors, which act as physiological attenuators of TNF-α 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.