Pathogenesis of rheumatoid arthritis

Studies into pathogenic mechanisms in rheumatoid arthritis have improved due to the transition from the premolecular to the molecular era. The chronic inflammatory destructive process in the synovial membrane has been proven to be highly complex with contributions of T cells, B cells, macrophages, and residual cells interlinked through a network of adhesion molecules, cytokines, and other mediators. Accumulating evidence suggests that a single hit model, as exemplified by the paradigm of an infectious organism being the causative agent, is too simplified, and that the involvement of nonimmune tissues and mechanisms has likely been underestimated. Progress in understanding the causes and pathogenesis of rheumatoid arthritis has come from the studies on genetic risk determinants. One of several suspected genetic risk factors has been mapped the HLA-DR B1 gene and has been shown to function as a progression factor in the disease process.