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Only a few years ago, little was known about the role of cytokines in rheumatoid arthritis. The original view of the cytokine milieu in the inflamed joint as a melange of factors from various cells was clarified by two observations.1 First, in inflammation of rheumatoid arthritis, cytokines from macrophages and fibroblasts dominate, and second, the cytokine profile within the macrophage and fibroblast reflects a hierarchy, with interleukin-1 and tumor necrosis factor α (TNF-α) assuming particular importance. Anticytokine therapy for rheumatoid arthritis has now reached the clinic, and the report in this issue of the Journal by Moreland et al.2 adds . . .
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Firestein et al. (1997) studied this question.
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