RT Journal Article SR Electronic T1 The IL23R Arg381Gln non-synonymous polymorphism confers susceptibility to ankylosing spondylitis JF Annals of the Rheumatic Diseases JO Ann Rheum Dis FD BMJ Publishing Group Ltd and European League Against Rheumatism SP 1451 OP 1454 DO 10.1136/ard.2007.080283 VO 67 IS 10 A1 B Rueda A1 G Orozco A1 E Raya A1 J L Fernandez-Sueiro A1 J Mulero A1 F J Blanco A1 C Vilches A1 M A González-Gay A1 J Martin YR 2008 UL http://ard.bmj.com/content/67/10/1451.abstract AB Objectives: Recent results have shown that the IL23R gene, coding for a subunit of the interleukin-23 receptor, is strongly associated with autoimmunity. The aim of the current study was to investigate, for the first time, the possible involvement of the IL23R gene in genetic susceptibility to ankylosing spondylitis (AS).Methods: We carried out a case–control association study in which 365 patients with AS and 500 blood bank donors were included. Eight single nucleotide polymorphisms (SNPs) spanning the IL23R gene were selected as genetic markers for our association study and were genotyped using a Taqman 5′ allelic discrimination assay.Results: Interestingly, we observed association of two of eight IL23R genotyped SNPs. The strongest effect was conferred by the non-synonymous rs11209026 (Arg381Gln) SNP (odds ratio 0.46 95% confidence interval 0.2 to 0.7 p = 0.001). Similarly, the IL23R rs1343151 SNP showed association with AS genetic susceptibility (odds ratio 0.68 95% confidence interval 0.55 to 0.83 p = 0.0002). After a conditional case–control test we observed that the effect of these two genetic variants was independent of linkage disequilibrium.Conclusions: These results suggest that the IL23R gene seems to be involved in AS genetic predisposition.