Progress in our understanding of the pathogenesis of ankylosing spondylitis

Abstract AS is a common rheumatic condition characterized by inflammation and new bone formation. The pathogenesis of AS is likely multifactorial and has not been fully elucidated to date. A major genetic role has been demonstrated. The strongest genetic association is with HLA B27. Numerous other a...

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Bibliographic Details
Published in:Rheumatology (Oxford, England) England), 2018-11, Vol.57 (suppl_6), p.vi4-vi9
Main Authors: Simone, Davide, Al Mossawi, M Hussein, Bowness, Paul
Format: Article
Language:English
Subjects:
Gastrointestinal Microbiome
Genetic Predisposition to Disease - genetics
HLA-B27 Antigen - genetics
Humans
Interleukin-17 - genetics
Interleukin-23 - genetics
Polymorphism, Genetic
Reviews
Spondylitis, Ankylosing - genetics
Spondylitis, Ankylosing - microbiology
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Summary:Abstract AS is a common rheumatic condition characterized by inflammation and new bone formation. The pathogenesis of AS is likely multifactorial and has not been fully elucidated to date. A major genetic role has been demonstrated. The strongest genetic association is with HLA B27. Numerous other associated genetic polymorphisms have been identified, including those affecting the type 17 immune pathway, although the precise link between genetics and pathogenesis remains unexplained. Several immunological alterations, together with recent therapeutic advances, support a central role for IL-23- and IL-17-producing immune cells in disease pathogenesis. Recently, perturbations of gut microbiota of AS patients have further catalysed research and offer potential for future therapeutic intervention. In this review we outline the genetic basis of AS and describe the current hypotheses for disease pathogenesis. We synthesize recent experimental research data and clinical studies to support a central role for the type 17/23 immune axis in AS.
ISSN:1462-0324
1462-0332
DOI:10.1093/rheumatology/key001