ASSOCIATION ANALYSIS IN RHEUMATOID ARTHRITIS OF GENES PREVIOUSLY ASSOCIATED TO SYSTEMIC LUPUS ERYTHEMATOSUS

Background: Rheumatoid Arthritis (RA) and systemic lupus erythematosus (SLE) share some genetic factors like the HLA, PTPN22, IRF5 and STAT4 genetic variants. Now, it is possible to examine more completely the extent of the commonality of their genetic component. Objectives: We aimed to test if other SLE genetic factors besides the 4 mentioned could be also implicated in RA susceptibility. Methods: A SNP in each of the genetic factors ITGAM (rs1143679), C8orf13-BLK (rs13277113), TYK2 (rs2304256), 1q25.1 (rs10798269), PXK (rs6445975), KIAA1542 (rs4963128), MECP2 (rs17435), BANK1 (rs17266594), and LY9 (rs509749) was studied in 1635 RA patients and 1626 controls from Spain. Genotyping was carried out using the SNaPshot technique and statistical analyses were performed comparing case and control allele frequencies using Chi-square tests on 2 x 2 contingency tables. These analyses were also conducted after stratifying the samples by gender and by clinical features (anti-CCP and RF status, SE, rheumatoid nodules, radiographic changes, Sjögren syndrome (SS) and pneumonitis). Results: No association was found with any of the 9 SNPs. In addition, there were no significant differences between having or not each of the clinical features analyzed except for the BLK-C8orf13 SNP, which minor allele was less frequent in patients with SS (14.6% vs 22.4% in controls, P = 0.003). However, this result should be taken with caution because only 134 patients were included in this subgroup. Conclusion: None of the 9 recently identified SLE risk factors, showed association to RA. Therefore, the common genetic factors affecting the pathogenesis of these two disorders seem to be limited to a few examples, revealing that we still have an incomplete understanding of the complex mechanisms controlling immune responses and self-reactivity. Disclosure of Interest: None declaredCitation: Annals of the Rheumatic Diseases, volume 68, supplement 3, year 2009, page 182Session: Genomics, genetic basis of disease and HLA/T cell recognition (Poster Presentations )