rs10181656

Several tightly linked SNPs in the STAT4 gene have been linked to risk for risk haplotype for systemic lupus erythematosus (SLE). The strongest association is found for either of two perfectly linked SNP alleles, rs10181656(G) and rs7582694(C), both yielding an odds ratio of 1.71 in this study of ~700 Swedish SLE patients. The risk for SLE was also calculated to increase as a function of the total number of risk alleles for this SNP plus 2 others in the IRF5 gene. Compared to individuals with 0 or 1 risk alleles, the risk for SLE increased 1.82-fold for each additional risk allele from this group. The odds ratio for SLE is 2.08 (CI: 1.53-2.83) for carriers of 2 risk alleles, and goes up to 13.0 (CI: 3.78-44.3) for carriers of 5 or 6 risk alleles (compared to those with 0 or 1). Association of STAT4 with rheumatoid arthritis in the Korean population. Re-evaluation of putative rheumatoid arthritis susceptibility genes in the post-genome wide association study era and hypothesis of a key pathway underlying susceptibility. Specificity of the STAT4 genetic association for severe disease manifestations of systemic lupus erythematosus. STAT4 polymorphism is associated with early-onset type 1 diabetes, but not with late-onset type 1 diabetes. High-density genotyping of STAT4 reveals multiple haplotypic associations with systemic lupus erythematosus in different racial groups. Overlap of disease susceptibility loci for rheumatoid arthritis and juvenile idiopathic arthritis. Variation in STAT4 is associated with systemic lupus erythematosus in a Finnish family cohort. Investigation of rheumatoid arthritis susceptibility genes identifies association of AFF3 and CD226 variants with response to anti-tumour necrosis factor treatment. Evidence for STAT4 as a common autoimmune gene: rs7574865 is associated with colonic Crohn's disease and early disease onset. Genetic risk factors in lupus nephritis and IgA nephropathy--no support of an overlap. Abnormal Genetic and Epigenetic Changes in Signal Transducer and Activator of Transcription 4 in the Pathogenesis of Inflammatory Bowel Diseases.