Streptococcal Cell Wall Arthritis

A severe polyarthritis can be induced in female Lewis rats by intraperitoneal administration of sonicated cell walls derived from group A, B, and C streptococci (1) . This clinical disease is characterized by an acute phase, detected between days 1 and 4, and a chronic phase that occurs N3 wk after immunization . Similarities exist between this disease in rats and human rheumatoid arthritis (RA) . 1 As seen in RA, the incidence of cell wall-induced disease is greater in females than males; genetic factors play a key role in disease induction ; the disease is complement dependent ; the immune cells of cell wall-treated rats are IL-2 deficient ; and the clinical disease is remittive and relapsing (2-4) . Although a large number of T lymphocytes are present in the inflamed synovium of patients with RA, their role in the pathogenesis ofthe disease is not entirely clear (5, 6) . However, in animal models of arthritis, cell-mediated immunity to the inciting antigen appears to play a key role . Adjuvant-induced arthritis is a T cell-dependent lesion, and activated lymphocytes from adjuvant arthritic rats (7, 8) and a Mycobacterium tuberculosis (MT)-specific T cell clone (9) can passively transfer clinical and histological disease to naive syngeneic recipients . In addition, passive disease is not detected in rats treated with an anti-T cell antibody (10) . Type II collageninduced arthritis in rats can also be transferred to syngeneic animals by T cells (11, 12) . The role of T cells in the pathogenesis of streptococcal cell wall (SCW)-induced arthritis has also been extensively studied (13-15), but evidence for their role in the disease has been indirect . It has been demonstrated that the acute phase of the disease is T cell independent and the development of the chronic phase is T cell dependent . In addition, the chronic phase of the disease does not develop in athymic rats or in those treated with cyclosporin A. Histological studies conducted in this model indicate that the synovial tissue ofrats in the chronic phase ofdisease contains T cells (16) . Nondigestible cell wall fragments persist in the synovial tissue, and it has been