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The continuing saga of the aetiology and pathogenesis of joint destruction in rheumatoid arthritis (RA) has often led to reassessment of the working hypotheses created to explain the phenomenon. Initial and current models set a protagonistic role for inflammatory and autoimmune cellular mediators in RA, and this notion has been well supported by a plethora of experimental data. However, it may have been biased by the relatively more easy access to experimental and clinical data regarding immune cell function and also, perhaps, by the overenthusiasm with which it was felt cellular immunology could explain chronic immunopathologies. Even from early investigations, however, it has been clear that for arthritis development, inflammatory and autoimmune processes actively interacted with a network of non-immune cell types, and that it was the effector activities of these cell types that resulted in cartilage and bone attack. Although, until recently, the non-immune constituents of the synovial lining were regarded as mere targets of the inflammatory milieu and as secondary players in the development of disease, more recent data provide serious grounds for considering these cells as dominant players in the aetiopathogenesis of RA. The series of reviews on synovial fibroblasts (SFs) presented in this issue of Arthritis Research aims to refocus attention on our current knowledge of the biology of SFs and their possible involvement in the development of RA.