Abstract
Rheumatoid arthritis is a chronic destructive disease of joints, characterized by inflammation, synovial hyperplasia, and abnormal cellular and humoral immune responses. Although several types of cells have been proposed to trigger synovial inflammation, the etiologic process and pathogenesis of the disease remain controversial. But, as indicated by a recent study by Lee et al.,1 the mast cell is emerging as a key player in the erosive and inflammatory events leading to joint destruction (Figure 1).The inflammatory processes that result in rheumatoid arthritis are multifactorial, involving complex interactions among the cytokine network, autoantibodies, and the complement cascade. Various mediators are . . .