Levamisole maintains cyclophsophamide-induced remission in murine lupus erythematosus.

Antibodies to DNA in 14 month old male NZB/W F1 mice were markedly decreased after 4 weeks of cyclophosphamide therapy. A group of these mice and untreated controls subsequently received levamisole for 12 weeks. Antibodies to DNA returned to pretreatment levels within 8 weeks in animals receiving only cyclophosphamide, whereas levamisole treatment after cyclophosphamide delayed the reappearance of these antibodies. Glomerular immunoglobulin deposition and the degree of lymphocytic tissue infiltrate were decreased in animals receiving cyclophosphamide followed by levamisole as compared with non-treated control animals or those receiving cyclophosphamide or levamisole alone. In vitro T-cell mitogen reactivity was inversely correlated with the final DNA antibody titres of individual mice, suggesting a relationship between decreased autoantibody production and augmented cellular immunity. We discuss possible mechanisms by which levamisole may delay the reappearance of autoantibodies and decrease the histological evidence of lupus nephritis when given to New Zealand mice first treated with cyclophosphamide.