Immune regulation in adjuvant-induced arthritis: possible implications for innovative therapeutic strategies in arthritis.

Abstract

Adjuvant-induced arthritis (AIA), the first experimental arthritis model, was described in 1956 (1,2), at a time when experimental autoimmune diseases affecting the central nervous system, peripheral nervous system, thyroid, and eye had been described, and autoimmunity began to be considered a significant mechanism in the pathogenesis of organ-specific inflammatory disease (3,4). AIA, which appeared in rats immunized with Mycobacterium tuberculosis in oil, showed suggestive similarities in clinical onset and course, as well as the pattern of lesions in joints, skin, eye, and mucosae, to reactive arthritis associated with infection by enteric organisms (primarily gram-negative bacilli) (for review, see ref. 5). The intensified, precocious appearance of AIA lesions at joint or skin sites traumatized by various means suggested that the disease might represent a disseminated autoimmune response to a joint or connective tissue antigen (6). Indeed, AIA could be transmitted by transferring sensitized lymph node cells (7,8) or thoracic duct cells (9) from sensitized donors to normal recipients, without administering M tuberculosis to the latter group.