Autoimmune reactions and rheumatoid arthritis.

The reviewed data suggest with a high degree of certainty that IgG and IgG antibodies in immune complexes as well as native and denatured collagen type I, II, and III are autoantigens capable of inducing T cell activation in patients with RA. Proteoglycans and their derivatives seem to modify lymphocyte reactions in a largely non-specific way and their potential to activate T Lymphocytes in RA has still to be confirmed. The occurrence of activation products of T lymphocytes in synovial tissue incubates and synovial fluid of RA patients that is of lymphokines seems to be established. The major autoantibody synthesized by synovial tissue (ST) of seropositive and seronegative RA and juvenile RA patients is IgG- rheumatoid factor (RF) and in seropositive adult cases in addition IgM-Rf. Synthesis of various types of agglutinators by ST plasma cells of adult and juvenile RA patients is a distinct but less prominent feature--than synthesis of Rf. In addition indirect evidence suggests that RA-ST synthesizes to some degree antibodies directed against native and denatured collagen type I/II/III and antibodies directed against different nuclear antigens as well as immunoconglutinin. All these autoantibodies seem to participate in the immune complex formation in RA joints and to activate the complement system. The vast majority of immune complexes, however, consists of IgG-Rf/IgG antigen and--in seropositive RA--of IgM-Rf.