Genetic susceptibility to ankylosing spondylitis.

Ankylosing spondylitis is a highly heritable, common rheumatic condition, primarily affecting the axial skeleton. The association with HLA-B27 has been demonstrated worldwide, and evidence for a role of HLA-B27 in disease comes from linkage and association studies in humans, and transgenic animal mo...

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Main Authors: Sims, A, Wordsworth, B, Brown, M
Format: Journal article
Language:English
Published: 2004
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author Sims, A
Wordsworth, B
Brown, M
author_facet Sims, A
Wordsworth, B
Brown, M
author_sort Sims, A
collection OXFORD
description Ankylosing spondylitis is a highly heritable, common rheumatic condition, primarily affecting the axial skeleton. The association with HLA-B27 has been demonstrated worldwide, and evidence for a role of HLA-B27 in disease comes from linkage and association studies in humans, and transgenic animal models. However, twin studies indicate that HLA-B27 contributes only 16% of the total genetic risk for disease. Furthermore, there is compelling evidence that non-B27 genes, both within and outwith the major histocompatability complex, are involved in disease aetiology. In this post-genomic era we have the tools to help elicit the genetic basis of disease. This review describes methods for genetic investigation of ankylosing spondylitis, and summarises the status of current research in this exciting area.
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spelling oxford-uuid:bc37502f-716e-43bf-b5b8-3931df764ed92022-03-27T05:22:43ZGenetic susceptibility to ankylosing spondylitis.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:bc37502f-716e-43bf-b5b8-3931df764ed9EnglishSymplectic Elements at Oxford2004Sims, AWordsworth, BBrown, MAnkylosing spondylitis is a highly heritable, common rheumatic condition, primarily affecting the axial skeleton. The association with HLA-B27 has been demonstrated worldwide, and evidence for a role of HLA-B27 in disease comes from linkage and association studies in humans, and transgenic animal models. However, twin studies indicate that HLA-B27 contributes only 16% of the total genetic risk for disease. Furthermore, there is compelling evidence that non-B27 genes, both within and outwith the major histocompatability complex, are involved in disease aetiology. In this post-genomic era we have the tools to help elicit the genetic basis of disease. This review describes methods for genetic investigation of ankylosing spondylitis, and summarises the status of current research in this exciting area.
spellingShingle Sims, A
Wordsworth, B
Brown, M
Genetic susceptibility to ankylosing spondylitis.
title Genetic susceptibility to ankylosing spondylitis.
title_full Genetic susceptibility to ankylosing spondylitis.
title_fullStr Genetic susceptibility to ankylosing spondylitis.
title_full_unstemmed Genetic susceptibility to ankylosing spondylitis.
title_short Genetic susceptibility to ankylosing spondylitis.
title_sort genetic susceptibility to ankylosing spondylitis
work_keys_str_mv AT simsa geneticsusceptibilitytoankylosingspondylitis
AT wordsworthb geneticsusceptibilitytoankylosingspondylitis
AT brownm geneticsusceptibilitytoankylosingspondylitis