Progress in spondylarthritis. Immunopathogenesis of spondyloarthritis which cells drive disease 英文参考文献.docVIP

Available online /content/11/3/233 Review Progress in spondylarthritis Immunopathogenesis of spondyloarthritis: which cells drive disease? Lode Melis and Dirk Elewaut Department of Rheumatology, Ghent University Hospital, 0K12IB, De Pintelaan 185, 9000 Ghent, Belgium Corresponding author: Dirk Elewaut, dirk.elewaut@ugent.be Published: 25 June 2009 Arthritis Research Therapy 2009, 11:233 (doi:10.1186/ar2722) This article is online at /content/11/3/233 ? 2009 BioMed Central Ltd Abstract the different disease phenotypes could consecutively mani- fest in the same patient, (b) overlaps that make it impossible to distinguish between the different disorders are often seen, and (c) different disorders can affect different members of the same family. Apart from the presence of shared environmental factors, this familial aggregation can be explained for the most part by an important hereditary component in the pathogenesis of the disease. First-degree relatives of SpA patients are 40 times more likely than the general population to develop SpA [1,2]. 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-asso- ciated 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