No association of polymorphisms in the suppressor of cytokine signaling (SOCS)-3 with rheumatoid arthritis in the Chinese Han population.

Abstract

Suppressor of cytokine signaling (SOCS)-3 is a key negative regulator of cytokine signaling that inhibits the JAK/STAT signal transduction pathway; there are reports describing its role in attenuating arthritis through SOCS-3 overexpression. We examined the relationship between polymorphisms in the coding sequence and promoter region of SOCS-3 and rheumatoid arthritis (RA) in a Chinese Han population. Two single-nucleotide polymorphisms in the SOCS-3 5' region: -1044 C>A within the promoter region and rs12953258 (-920 C>A) in the 5'UTR (exon 2) of SOCS-3 were studied by restriction fragment length polymorphism analysis and tetra-ARMS-PCR in 100 RA patients and 100 healthy adults. The prevalence of the homozygous genotype -1044 CC was 100% in both RA and control groups. The heterozygous genotype (-920 C>A) was present in 89% of RA and in 82% of the control group, which is significantly different from the distribution in Western people. There was no transmission disequilibrium between these two SNPs (r(2) = 0.000). We did not detect significant differences in allele or genotype frequencies for either of these SNPs between the RA group and controls (P > 0.05). There was no association between rheumatoid factor and SOCS-3 SNP rs12953258 (P = 0.258). We conclude that SOCS-3 polymorphism is not a genetic risk factor for RA in Chinese patients.