The pathogenesis of rheumatoid arthritis: a guide to therapy.
The cause of rheumatoid arthritis (RA) is unknown; however, extensive research has yielded great insight into its pathogenesis. Lymphocytes play a significant role, but a lesser role in the perpetuation of late disease. The rheumatoid synovium is composed primarily of fibroblasts and monocytes that produce inflammatory cytokines, of which interleukin-1 and tumor necrosis factor are of key importance. Potential regulatory mechanisms balancing the effects of these cytokines are inadequate to prevent joint damage and subsequent disability. These cytokines seem responsible for stimulating destructive processes in the joint via induction of prostaglandins, angiogenesis, chemokines, adhesion molecules, osteoclastogenesis, and matrix metalloproteinases. This review discusses recent research findings in the immunopathogenesis of RA with respect to potential targets for therapy.
Jenkins
John K
JK
Department of Medicine, University of Mississippi Medical Center, Jackson 39216, USA. jjenkins@medicine.umsmed.edu
Hardy
Kenneth J
KJ
McMurray
Robert W
RW
D001172:Arthritis, Rheumatoid / Q000097:blood / Q000175:diagnosis* / Q000188:drug therapy* / Q000235:genetics; D001402:B-Lymphocytes / Q000378:metabolism; D002448:Cell Adhesion; D016207:Cytokines / Q000378:metabolism; D005347:Fibroblasts / Q000378:metabolism; D006801:Humans; D008954:Models, Biological; D013601:T-Lymphocytes / Q000378:metabolism
D016207:Cytokines