Pathogenesis of rheumatoid arthritis: how early is early?

Gary S Firestein

doi:10.1186/ar1780

Abstract

Studies of cytokine expression in rheumatoid arthritis have provided key insights into the pathogenesis of disease and have offered clues for effective therapy. Patterns of T-cell products in chronic rheumatoid synovitis suggest that T helper type 1 cells contribute to the perpetuation of disease. However, there is no guarantee that the mechanisms of late disease are identical to very early rheumatoid arthritis. Evaluation of the cytokine profile at the earliest time points after onset of symptoms could identify novel targets that prevent progression to chronic arthritis.

Highlights

Development of hypotheses to explain the pathogenesis of chronic rheumatoid arthritis (RA), including the interesting new study by Raza and colleagues [1], has been a wondrous adventure
Chronic rheumatoid synovitis is marked by a complex interplay between multiple cell types, and individual patients display their own distinct hierarchy for the efficacy of therapeutic interventions [4]
The lymphocyte cytokine profile in chronic RA synovium and surface chemokine receptor display is most consistent with a T helper cell type 1 (Th1)-driven disease [5]

Summary

Introduction

Development of hypotheses to explain the pathogenesis of chronic rheumatoid arthritis (RA), including the interesting new study by Raza and colleagues [1], has been a wondrous adventure. Chronic rheumatoid synovitis is marked by a complex interplay between multiple cell types, and individual patients display their own distinct hierarchy for the efficacy of therapeutic interventions [4]. The nature of this response remains poorly defined, and studies of chronic rheumatoid synovitis have generally demonstrated blunted Tcell function and surprisingly limited cytokine production compared with other T-cell-mediated diseases.

Results

Conclusion