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Progress in spondylarthritis. Immunopathogenesis of spondyloarthritis: which cells drive disease?

Lode Melis and Dirk Elewaut*

Author Affiliations

Department of Rheumatology, Ghent University Hospital, 0K12IB, De Pintelaan 185, 9000 Ghent, Belgium

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Arthritis Research & Therapy 2009, 11:233  doi:10.1186/ar2722

Published: 25 June 2009


Spondyloarthritides, or SpA, form a cluster of chronic inflammatory diseases with the axial skeleton as the most typical disease localisation, although extra-articular manifestations such as intestinal inflammation may frequently occur during the course of the disease. This review summarises recent progress in our understanding of the immunopathogenesis of SpA with special emphasis on the cellular constituents considered to be responsible for the initiation and/or perpetuation of inflammation. There are several arguments favouring a role for haematopoietic cells in the pathophysiology of spondyloarthritis, including HLA-B27-associated dendritic cell disturbances, HLA-B27 misfolding properties and T helper 17 cells. In addition, recent studies have pointed toward a pivotal role for stromal cells. A major challenge, however, remains to determine how recently identified genetic associations such as interleukin-23 receptor polymorphisms may influence cellular targets in spondyloarthritis.