rs1738074

This meta-analysis of 22,233 CAD cases and 64,762 controls tested 41 celiac disease-associated SNPs for association with coronary artery disease (CAD). While 58.5% of celiac disease risk alleles showed positive association with CAD (OR 1.001-1.081), this was not significantly different from the 50% expected by chance (p=0.069). Only rs653178 at the SH2B3/ATXN2 locus achieved study-wide statistical significance (OR 1.081, p=2.2×10⁻⁶), likely through pleiotropic effects. The findings provide no convincing evidence that genetic variants associated with celiac disease contribute to CAD risk.

This case-control study of 446 African-American RA patients and 733 controls identified three SNPs significantly associated with rheumatoid arthritis: TNFAIP3 rs719149 (A allele OR 1.22, p=0.02), TAGAP rs1738074 (G allele OR 0.75, p=0.0012), and TAGAP rs4709267 (G allele OR 0.74, p=0.004). Conditional analyses suggest the two TAGAP SNPs have independent effects despite weak linkage disequilibrium (R²=0.034).

This meta-analysis of 7 genome-wide association studies identified three novel multiple sclerosis susceptibility loci: rs170934 near EOMES (3p24.1, OR=1.17, P=1.6×10⁻⁸), rs2150702 in MLANA (9p24.1, OR=1.16, P=3.3×10⁻⁸), and rs6718520 near THADA (2p21, OR=1.17, P=3.4×10⁻⁸). The analysis encompassed 5,545 cases and 12,153 controls and identified 10 additional loci with suggestive evidence of association (P<1×10⁻⁶), including IL12B, TAGAP, PLEK, and ZMIZ1, which are shared with other inflammatory diseases.

A meta-analysis of 4,107 type 2 diabetes cases and 5,187 controls from three GWA studies found no evidence that common variants altering circulating inflammatory protein levels (IL-18, IL-6R, CRP, IL1RN, PAI1, MIF) or variants predisposing to autoimmune diseases (type 1 diabetes, rheumatoid arthritis, Crohn's disease, celiac disease, multiple sclerosis, SLE) are associated with type 2 diabetes risk. For example, rs2250417 in IL18 showed OR=1.00 (95% CI 0.99-1.03) versus the expected OR of ~1.15 if inflammation were causal, suggesting inflammatory markers are likely secondary rather than causative in type 2 diabetes.