Immunopathogenesis of Rheumatoid Arthritis: insights from animal models and the clinic

摘要

Rheumatoid Arthritis (RA) is a chronic, systemic inflammatory disease characterized primarily by a symmetrical, destructive, polyarthritis. Histologic analysis of RA joint tissue reveals marked hypertrophy of the synovium with a mononuclear inflammatory infiltrate. This hyperplastic synovial tissue, termed pannus, locally invades tendons, subchondral bone, and articular cartilage, leading to joint dysfunction and in some cases, joint destruction. While the etiology of RA remains obscure, the diseaseappears to represent the end product of the interplay of predisposing genetic factors and environmental triggers. Localization of the inflammatory process to joint suggests that the process may represent an example of organ specific autoimmunity to as yet undefined antigen(s) preferentially expressed at the site.