Cyclophosphamide intensifies the acquisition of allergic contact dermatitis in mice rendered B-cell deficient by heterologous anti-IgM antisera.
Treatment with cyclophosphamide (Cy) before contact sensitization regularly intensifies the induced sensitivity. The immunopotentiation is specific and appears due to toxicity for suppressor cells. It has been proposed that the target of Cy immunopotentiation is a suppressor B cell. We have studies allergic contact dermatitis (ACD) in mice rendered B-cell deficient by chronic treatment, beginning at birth, with a goat antiserum against mouse IgM. The ACD induced in these B-cell deficient mice was equal to that induced in intact mice. The hypersensitivity was readily and equally immunopotentiated by Cy in normal and in B-cell deficient mice. It appears that the suppressor cell that is the target of Cy immunopotentiation is not a B cell but rather a T cell.
D000818:Animals; D000917:Antibody Formation / Q000187:drug effects; D001402:B-Lymphocytes / Q000276:immunology*; D003520:Cyclophosphamide / Q000494:pharmacology*; D003877:Dermatitis, Contact / Q000209:etiology*; D005260:Female; D007106:Immune Sera; D007075:Immunoglobulin M / Q000276:immunology*; D007165:Immunosuppression Therapy; D008212:Lymphocyte Depletion; D051379:Mice; D013601:T-Lymphocytes / Q000187:drug effects; D013997:Time Factors
D007106:Immune Sera; D007075:Immunoglobulin M; D003520:Cyclophosphamide