ABSTRACT
JOHN W. WHITAKER, ROBERT SHOEMAKER, DAVID L. BOYLE, JOSH HILLMAN, DAVID ANDERSON, WEI WANG, AND GARY S. FIRESTEIN
12.1 BACKGROUND
RA is a chronic inflammatory disease marked by synovial hyperplasia and invasion into cartilage and bone. This process is mediated, in part, by cytokines like IL-1, IL-6, and TNF that activate a broad array of cell signaling mechanisms and leads to the release of destructive enzymes [1]. Fibroblast-like synoviocytes (FLS), which form the inner lining of the synovium, play an active role in joint destruction by invading intraarticular cartilage and other support structures of the joint [2]. These mesenchymal cells normally produce hyaluronic acid and other lubricants that facilitate joint movement and a low friction environment.
