Cell-mediated immunity in rheumatic disease

Rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis are the three most common systemic rheumatic diseases in which disordered immune function is thought to play a pathogenetic role. Each disease has different and characteristic abnormalities of the cellular immune system. In rheumatoid arthritis the identified abnormalities of immunoregulation are largely limited to specific antigens: Epstein-Barr virus and collagen. Systemic lupus erythematosus is characterized by exuberant B-cell activity with exaggerated humoral response, a diversity of autoantibodies, non-antigen-specific loss of suppressor cell function, and general suppression of cell-mediated immunity. In systemic sclerosis systemic defects of cellular and humoral immune function are mild, but the release of lymphokines and monokines at sites of inflammatory lesions is thought to be important in the pathogenesis of the disease. Similar immune cell-connetive tissue cell interactions are probably important in the propagation of rheumatoid synovitis. Thus, despite the many shared clinical and serologic features of these diseases as well as the presence of many patients who have clinically overlapping features of more than one of these entities, the immune defects and the immunopathogenesis of these disorders appear to be distinct.