Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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

Mol Immunol

Publication Date

01/2014

Volume

57

Pages

38 - 43

Keywords

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