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Published on: March 14, 2016
The -383A>C TNFRI polymorphism is associated with soluble levels and clinical activity in rheumatoid arthritis
Y Valle1, J R Padilla-Gutiérrez, N M Torres-Carrillo
1Departamento de Biología Molecular y Genómica, Centro Universitario de Ciencias de la Salud, Instituto de Investigación en Reumatología y del Sistema Músculo Esquelético, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico.
Abstract:
Tumor necrosis factor-alpha (TNF-alpha) plays a central role in inflammation, and it has been directly implicated in the pathogenesis of rheumatoid arthritis (RA). TNF-alpha activity is mediated through TNFRI and TNFRII cell surface receptors, which act as physiological attenuators of TNF-alpha 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.
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