ABSTRACT
An autoimmune process is thought to underlie articular manifestations of diseases, i.e., rheumatic fever, rheumatoid arthritis, ankylosing spondylitis, Reiter’s syndrome, and other forms of reactive arthritis. The most direct evidence for the responsibility of mycobacteria in the etiology of autoimmune arthritis, however, stems from studies of adjuvant arthritis (AA), a prototype of autoimmune arthritis triggered by bacterial antigens. Pathogenesis of certain forms of autoimmune arthritis remains unclear. Some investigators have suggested that formation of immune complexes by rheumatoid factor is responsible for rheumatoid synovial inflammation. The lesson of AA is that an experimental autoimmune arthritis can be triggered by immunization to a mycobacterial antigen that shares an epitope with a self-component. The basic concept behind the use of T-lymphocyte lines for studying autoimmunity is a reminiscent of Koch’s postulates for infectious diseases. T-lymphocyte lines and clones can be effectively used for preventing imminent or treating ongoing autoimmune arthritis.
