ABSTRACT
RICHARD M. POPE, BARBARA DREVLOW, JENNIFER CAPEZIO, and ROSA LOVIS Northwestern University Medical School, Chicago, Illinois
ALAN LANDAY Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois
I. INTRODUCTION
Interleukin-I ) is a mediator of the inflammation that may be important in rheumatoid arthritis (RA). It is produced locally by synovial lining cells and by synovial tissue macrophages. Locally produced IL-I may contribute to the pathogenesis of RA by stimulation of the secretion of stromelysin and collagenase by fibroblasts. Furthermore, IL-I contributes to the induction of other inflammatory cytokines by macrophages and fibroblasts, including IL-8, TNF-a, and IL-6 (reviewed in Ref. I). Natural inhibitors of [L-1, including [L-1 receptor (IL-IR) and [L-l R antagonist I -Ra), are produced locally in inflammatory sites in an attempt to down-regulate the activity of IL-I (2-4). Nevertheless, an imbalance between IL-I and its inhibitors may still occur and contribute to the chronic inflammation.
