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See Latest ArticlesGenetics and the pathogenesis of ankylosing spondylitis
Current Opinion in Rheumatology, 06/11/09
Brown MA et al. - Convincing evidence has been reported for the existence of further non-B27 MHC genes involved in AS. Strong, replicated association has been reported with IL23R and ERAP1 and AS. The IL23R finding strongly implicates the TH17 lymphocyte system in AS aetiopathogenesis. Suggestive evidence of a role for KIR gene polymorphism in AS exists.
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