AB0016 GENETIC VARIANTS OF PREDISPOSITION TO RHEUMATOID ARTHRITIS IN BELARUSIAN POPULATION

Background Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by autoimmune response focused in the synovium. RA complex disorder with significant genetic component and it also known to have possible environmental triggers. Microbiota bacterial infections play role etiology. The onset of may be accompanied previous or ongoing chlamydia infection some cases. Objectives determine variants susceptibility Belarusian population Methods 650 individuals were divided into 2 cohorts: 305 patients (59.69 ± 12.20), 345 controls (mean age 37.42 10.62). Patients further stratified two subsets – those catamnestic Chlamydia trachomatis/Chlamydophila pneumoniae (43, “RAChl+”) without (262, “RAChl-“). 11 SNPs 10 genes ( IL6 (rs1800795), IL6R (rs2228145 rs4845618), STAT4 (rs7574865), TRAF1/C5 (rs3761847), RUNX1 (rs9979383), RUNX3 (rs11249215), PTPN2 (rs2542151), PTPN22 (rs2476601), AGER (rs1035798), SLC7A11 (rs13128867)) genotyped using Real-time PCR PCR-RFLP. Results It was found that homozygous TT genotype at rs7574865 locus gene CT+TT genotypes rs2476601 are associated general (OR 2.71 [1.31 5.61]; p = 0.005 OR 2.47 [1.75-3.48] p<0.000, respectively). CC rs9979383 AG+GG rs11249215 revealed protective effect 0.63 [0.40-0.98] p=0.036 0.58 [0.36-0.92] p=0.02, lack association shown for polymorphic loci rs4l45618), (rs13128867), (rs2542151) (rs3761847) genes. For according presence/absence C. trachomatis/C. rs1800795 AA specifically risk developing infection-associated 5.22 [1.85–14.71] p=0.0024 2.63 [1.09-6.35] p=0.037). In addition, TG+GG rs2542151 RAChl+ clinical phenotype (2.10 [1.10-3.99] p=0.025). No either subtypes (rs2228145, (rs13128867) , (rs3761847). Conclusion Thus, key autoimmunity, gene, involved JAK/STAT pathway immune response, increase cohort population. At same time, its product being central proinflammatory cytokine, T-cell initiated as well signaling pathways through activation, only phenotype. Our data indicate contribute basis pathogenesis renewal response. Acknowledgements This research supported Research Technical Program “DNA Identification” (2017–2021), project number: 6.4 Disclosure Interests None declared