Immunosuppression as a desired pharmacological effect.
The immunosuppressive efficacy of the antineoplastic antibiotic Aclacinomycin A (ACM) was assayed in several test models for humoral and cellular immune response. Humoral immune response, measured as splenic plaque forming cells (PFC) in vitro and in vivo was markedly inhibited by ACM. Suppression of PFC in vivo could be observed when ACM was administered together with the antigen, or three days later. Concomitantly a decrease of circulating antibodies to SRBC was obtained. No effect on T-cell mediated immune response - DTH reaction and allogeneic cytotoxic lymphocytes - or on skin transplantation or a T-cell mediated autoimmune disease, EAE, was observed. ACM beneficially influenced the course of the disease in two GvH-models (hemolytic anemia and immune complex glomerulonephritis) which lead to a B-cell mediated autoimmune disease with fatal outcome. It was concluded that the therapeutic effect of ACM on GvH-disease is mediated via its suppression of the B-cell response.
D015250:Aclarubicin / Q000031:analogs & derivatives*; D000743:Anemia, Hemolytic / Q000188:drug therapy / Q000276:immunology; D000818:Animals; D000903:Antibiotics, Antineoplastic / Q000494:pharmacology*; D000917:Antibody Formation / Q000187:drug effects; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology; D005260:Female; D005921:Glomerulonephritis / Q000188:drug therapy / Q000276:immunology; D006086:Graft vs Host Disease / Q000188:drug therapy / Q000276:immunology; D006462:Hemolytic Plaque Technique; D007105:Immune Complex Diseases / Q000188:drug therapy; D007111:Immunity, Cellular / Q000187:drug effects; D007166:Immunosuppressive Agents / Q000494:pharmacology*; D051379:Mice; D008815:Mice, Inbred Strains; D009279:Naphthacenes / Q000494:pharmacology; D051381:Rats; D011917:Rats, Inbred Lew
D000903:Antibiotics, Antineoplastic; D007166:Immunosuppressive Agents; D009279:Naphthacenes; C011157:aclacinomycins; D015250:Aclarubicin