1858 C/T Polymorphism of the Protein Tyrosine Phosphatase Nonreceptor 22 Gene and Rheumatoid Arthritis Risk in Europeans: A Meta-analysis

Background and Aims le nucleotide polymorphism (SNP) of the protein tyrosine phosphatase nonreceptor gene (PTPN22) confers susceptibility to rheumatoid arthritis (RA) and certain other classical autoimmune diseases. The association between PTPN22 1858C/T polymorphism and the risk of RA is still controversial and ambiguous; therefore, we performed this meta-analysis to confirm some relationships. s ducted a search in the PubMed database without a language limitation, covering all papers published until June 20, 2011. Overall, 19 case-control studies with 11,727 cases and 12,640 controls were retrieved based on the search criteria for RA susceptibility related to the 1858C/T polymorphism. Odds ratios (OR) and 95% confidence intervals (CI) were used to assess the strength of this association. Publication bias was assessed with Eggers test. s nd that PTPN22 1858C/T polymorphism could increase RA risk in overall genetic models in Europeans (T-allele vs. C-allele, OR = 1.54, 95% CI = 1.47–1.62, Pheterogeneity = 0.143; TT vs. CC, OR = 2.86, 95% CI = 2.29–3.57, Pheterogeneity = 0.302; TC vs. CC, OR = 1.45, 95% CI = 1.38–1.53, Pheterogeneity = 0.273; TT + TC vs. CC, OR = 1.49, 95% CI = 1.42–1.56, Pheterogeneity = 0.208; TT vs. TC + CC, OR = 2.52, 95% CI = 1.95–3.25, Pheterogeneity = 0.296). Furthermore, significant relationships were detected among PTPN22 1858C/T polymorphism and RF+ or RF− RA risk. No obvious evidence of publication bias was detected in the overall analysis. sions udy indicated that PTPN22 1858T allele was significantly associated with increased RA risk.