The - 383A>C TNFRI polymorphism is associated with soluble levels and clinical activity in rheumatoid arthritis

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.