Immunopathogenesis of rheumatoid arthritis

摘要: From the Department of Medicine, The Division Rheumatic Diseases, Hospital for Special Surgery, New York Hospital-Cornell University Medical Center and Rockefeller University. Work carried out in Dr. Paget’s laboratory was supported by USPHS Grant AM 14627 an Arthritis Foundation Fellowship. Gibofsky 05766. Requests reprints should be addressed to Stephen A. Paget. 535 East 70th Street, York, 10021. Manuscript accepted July 24,1979. Compelling evidence implicates genetically controlled immunologic processes initiation perpetuation inflammatory events characteristic rheumatoid arthritis. Presently, it is believed that arthritis arises through immunopathologic responses as yet unidentified antigen, possibly related atypical microbial infection, susceptible host. Both humoral cell-mediated immune appear participate immunopathogenesis It thought extensive antigen-stimulated Tand B-lymphocyte macrophage interactions take place within synovial membrane. This results release lymphokines from T-cells immunoglobulins plasma cells. Such antibody can form complexes interacting with antigen or, case immunoglobulin G (IgG) factor, self-association. Immune play a significant initiating role process enzymatic cartilege degradation interaction complement components. Rheumatoid viewed disorder regulation which immunopathology failure coordinate functions response certain antigens. demonstration alteration suppressor cell populations well diminished skin test mitogen responsiveness support this view. T-lymphocyte predominance membrane clinical improvement patients treated thoracic duct drainage predominantly T-lymphocytes further stress disease. Recent data indicates susceptibility inherited trait, determined gene products major histocompatibility system. demonstrated significantlv increased frequency particular B-cell alloantigens seropositive patients. Control will require understanding its complex immunogenetics. Paget: term ‘rheumatoid arthritis, introduced Garrod 1859, describes systemic disease characterized clinically female predominance, symmetrical polyarthropathy morning stiffness factor positivity 80 per cent course highly variable: some, manifestations are mild; others, progresses rapidlv severe disability [I]. To social impact into