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Rheumatology Advance Access originally published online on March 27, 2006
Rheumatology 2006 45(6):669-675; doi:10.1093/rheumatology/kel065
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© The Author 2006. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

REVIEW

Synovial fibroblasts: key players in rheumatoid arthritis

L. C. Huber, O. Distler, I. Tarner1, R. E. Gay, S. Gay and T. Pap2

Center of Experimental Rheumatology, University Hospital Zurich, Switzerland, 1 Department of Internal Medicine and Rheumatology, Justus-Liebig University Giessen, Kerckhoff-Clinic, Bad Nauheim and 2 Division of Molecular Medicine of Musculoskeletal Tissue, University Hospital Munster, Germany.

Correspondence to: L. Huber, Center of Experimental Rheumatology, Department of Rheumatology, University Hospital Zurich, Gloriastrasse 23CH-8091 Zürich, Switzerland. E-mail: lars.huber{at}usz.ch

Rheumatoid arthritis (RA) is a chronic autoimmune-disease of unknown origin that primarily affects the joints and ultimately leads to their destruction. The involvement of immune cells is a general hallmark of autoimmune-related disorders. In this regard, macrophages, T cells and their respective cytokines play a pivotal role in RA. However, the notion that RA is a primarily T-cell-dependent disease has been strongly challenged during recent years. Rather, it has been understood that resident, fibroblast-like cells contribute significantly to the perpetuation of disease, and that they may even play a role in its initiation. These rheumatoid arthritis synovial fibroblasts (RASFs) constitute a quite unique cell type that distinguishes RA from other inflammatory conditions of the joints.

A number of studies have demonstrated that RASFs show alterations in morphology and behaviour, including molecular changes in signalling cascades, apoptosis responses and in the expression of adhesion molecules as well as matrix-degrading enzymes. These changes appear to reflect a stable activation of RASFs, which occurs independently of continuous exogenous stimulation. As a consequence, RASFs are no longer considered passive bystanders but active players in the complex intercellular network of RA.


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