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The spondyloarthropathies represent highly enigmatic conditions and although their clinical features, anatomical distribution of disease and genetic predisposing factors have been known for some time, a unified concept of the basic pathobiology underlying these illnesses has remained undefined. Recently progress has been made because numerous independent studies have converged upon IL-23 as a central cytokine in spondyloarthropathy and the mechanism and sites of action of this cytokine have now become much clearer. These findings enable the rational design of therapeutic strategies which it is hoped will profoundly modify the progression of these diseases. We will review the anatomical sites affected and the evidence for the importance of IL-23 in these conditions, before drawing these lines of investigation together to propose a model for the unified understanding of spondyloarthropathy.

Original publication

DOI

10.1016/j.molimm.2013.06.010

Type

Journal article

Journal

Molecular immunology

Publication Date

01/2014

Volume

57

Pages

38 - 43

Addresses

University of Birmingham, Edgbaston, Birmingham B15 2TT, UK; Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, OX3 7HE, UK. Electronic address: jonsherlock1-bd@yahoo.co.uk.

Keywords

Bone and Bones, Spine, Joints, Animals, Humans, Spondylitis, Ankylosing, Genetic Predisposition to Disease, HLA-B27 Antigen, Interleukin-23