REPORT

New targets IV

Defining a role for fibroblasts in the persistence of chronic inflammatory joint disease

C D Buckley, A Filer, O Haworth, G Parsonage, M Salmon

Rheumatology Research Group, Division of Immunity and Infection, Institute of Biomedical Research, MRC Center for Immune Regulation, University of Birmingham, Birmingham, UK

Correspondence to:
Correspondence to:
C D Buckley
Department of Rheumatology, Division of Immunity and Infection, University of Birmingham, Birmingham, B15 2TT, UK; c.d.buckley{at}bham.ac.uk

The most surprising feature of the inflammatory response in rheumatoid arthritis is not that it occurs but that it does not resolve. The persistence of the chronic inflammatory response in conjunction with ongoing joint destruction is an all too familiar finding in many patients with rheumatoid arthritis. Despite the use of effective anti-inflammatory agents and disease modifying drugs, a significant proportion of patients with rheumatoid arthritis continue to have resistant disease. Complete clinical remission is unusual for more than six months and a formal cure of the disease remains elusive. In this report we focus on how attempts to address the question of why rheumatoid arthritis persists have led to a different interpretation of the pathogenesis of rheumatoid disease; one in which alterations in stromal cells such as fibroblasts play an important role in the switch from resolving to persistent disease.

Keywords: rheumatoid arthritis; inflammation; fibroblasts

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