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FRI0426 No demonstrable effect of IL-23 receptor variants on clinical measures and IL23/ IL-17 levels in ankylosing spondylitis
  1. J Nossent1,2,
  2. S Johnsen3,
  3. G Bakland2,4
  1. 1School of Medicine, University of Western Australia, Crawley, Australia
  2. 2Bone and Joint Group, Arctic University, Tromso
  3. 3Norwegian University of Life Sciences, Ås
  4. 4Rheumatology, University Hospital North Norway, Tromso, Norway


Background IL23 binding to IL23 receptor (IL23R) is necessary for the maturation of Th17 cells and generation of proinflammatory IL17 and TNF in AS. IL23R variants have considerable impact on AS susceptibility in genome-wide association studies.

Objectives To describe the effect of genotypic IL23R variants on proinflammatory cytokines and disease measures in AS.

Methods Cross sectional cohort study of patients with established AS (n=334, 90% B27 +, mean age at study 45 years) included in a disease registry. IL23R genotyping for nonsynonymous SNP's (rs11209026 (protective allele A) and rs11209032 (risk allele A) was done by Taqman RT-PCR, while IL23, IL17, IL6 and TNF levels determined by sandwich ELISA and compared with age and gender matched healthy controls (n=72). Genotypic associations with clinical and serological features were analyzed with nonparametric methods.

Results There was no significant difference between in AS patients and controls regarding IL23 (276 vs 262 pg/ml, p>0.4) and IL17 levels (184 vs 233 pg/ml, p>0.2). Only 22 (6.6%) AS patients carried the protective rs11209026 A allele, while 206 (61.7%) carried the rs11209032 A risk allele (p=0.03). There was no demonstrable influence of individual genotypes (A vs G, AA vs AG vs GG) or haplotypic combinations on BASFI, spinal function tests, CRP, ESR, IL-23 or IL-17 levels (all p>0.3)

Conclusions While there is a high prevalence of the IL-23R rs11209032 A risk allele in Caucasian AS patients, this has no demonstrable bearing on clinical disease measures or serum IL-23 and IL-17 levels.

Acknowledgements The authors wish to acknowledge the technical assistance by mrs K Nilsen and the financial support of the North Norwegian Health Authority Research Fund

Disclosure of Interest None declared

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