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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.

Original publication

DOI

10.1016/s0889-857x(05)70045-4

Type

Journal article

Journal

Rheumatic diseases clinics of North America

Publication Date

11/1998

Volume

24

Pages

845 - 863

Addresses

Nuffield Department of Clinical Medicine, Wellcome Trust Centre for Human Genetics, Nuffield Orthopaedic Centre, United Kingdom. paul.wordsworth@well.ox.ac.uk

Keywords

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