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Ankylosing spondylitis is a highly genetic disease, with up to 98% of the population variance genetically determined. The major genetic effect arises from HLA-B27, but other HLA class I molecules, including HLA-B60, also play a role. HLA class II association may indicate either an independent effect for these genes or the existence of extended MHC haplotype containing other relevant genetic loci. The HLA-linked component of the genetic contribution to AS is substantially less than 50%, and preliminary analysis of affected sibling pairs by whole genome screening has revealed several potential regions of interest. The next 5 years should lead to the confirmation of some of these linkages, their refinement, and the testing of candidate genes within them. Ultimately, a better understanding of the genetic etiology of AS should yield insight into the pathogenic mechanisms and the development of novel strategies for treatment and prevention.


Journal article


Rheum Dis Clin North Am

Publication Date





845 - 863


Genetic Testing, HLA-B27 Antigen, Humans, Spondylitis, Ankylosing