Pathogenetic difference between collagen arthritis and adjuvant arthritis.

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Abstract
Daily treatment with cyclosporin at a dose of 25 mg/kg for 14 d [days] gave complete suppression of the development of collagen arthritis and adjuvant arthritis in Sprague-Dawley rats during an observation period of 45 d. To study whether the immunologic unresponsiveness produced by cyclosporin is antigen specific, the cyclosporin-protected rats were rechallenged with either type II collagen or complete Freund''s adjuvant (CFA) after discontinuation of cyclosporin treatment. Type II collagen-immunized cyclosporin-protected rats did not develop arthritis in response to reimmunization with type II collagen, but they did develop arthritis in response to a subsequent injection of CFA. CFA-injected, cyclosporin-protected rats showed a suppressed arthritogenic reaction in response to reinjection of CFA, whereas their response to a subsequent immunization with type II collagen was unaffected. The rats that were treated with cyclosporin without any prior antigenic challenge could develop arthritis in response to a subsequent injection of CFA or type II collagen after cessation of cyclosporin treatment. Specific immunologic unresponsiveness can be induced by cyclosporin in the 2 experimental models of polyarthritis, collagen arthritis and adjuvant arthritis. There is no cross-reactivity between type II collagen and the mycobacterial cell wall components. Immunity to type II collagen plays a critical role in the pathogenesis of collagen arthritis but its pathogenetic role in adjuvant arthritis is insignificant.
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