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C Arita

Publications and source records attributed to C Arita.

23 records · Page 2Linked to original sources
PubMed1985

Serum transfer of collagen arthritis in congenitally athymic nude rats.

The role of cellular immunity in collagen arthritis was investigated with congenitally athymic nude rats (rnu/rnu) and their heterozygous littermates (rnu/+). Immunization with type II collagen induced polyarthritis and definite immunity to type II collagen in rnu/+ rats, whereas rnu/rnu rats did not develop arthritis or immunity to collagen. An additional study demonstrated that collagen arthritis could be passively transferred with a serum concentrate from arthritic Sprague-Dawley rats to naive rnu/rnu rats as well as to rnu/+ rats. Histopathologically, the passively transferred arthritis in rnu/rnu rats resembled that in rnu/+ rats. Despite no difference in clearance of anti-type II collagen antibody after transfer between them, the passively transferred arthritis in rnu/rnu rats was significantly enhanced and prolonged in comparison with that in rnu/+ rats. These results indicate that arthritis may be inducible by humoral immunity in the absence of functional T cells and also suggest that anti-type II collagen-antibody is not the sole regulatory factor and that the suppressor cell system might regulate the clinical course of the disease.

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PubMed1984

Pathogenetic difference between collagen arthritis and adjuvant arthritis.

Daily treatment with cyclosporin at a dose of 25 mg/kg for 14 d 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, we rechallenged the cyclosporin-protected rats 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. Similarly, 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. On the other hand, 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. These results indicate that specific immunologic unresponsiveness can be induced by cyclosporin in the two experimental models of polyarthritis, collagen arthritis and adjuvant arthritis, and that there is no cross-reactivity between type II collagen and the mycobacterial cell wall components. The results further indicate that immunity to type II collagen plays a critical role in the pathogenesis of collagen arthritis but that its pathogenetic role in adjuvant arthritis is insignificant.

Animals↗