Aclacinomycin (ACM) a new cytotoxic antibiotic employed in cancer chemotherapy, can either enhance or inhibit the NK-cell activity of the immune system, depending on the dose administered. A single intraperitoneal injection of 2–4 mg/kg of ACM augments the cytolytic activity by spleen and peritoneal exudate cells of normal mice and spleen cells depleted of nylon-adherent cells and peritoneal exudate cells of tumor-bearing mice. In contrast to the stimulatory effect of NK-cell activity by low doses of ACM, a single injection of 8 mg/kg of this agent leads to depression in the level of NK-cell activity in both normal and tumor-bearing animals. We suggest that the mechanism through which the ACM enhances NK-cell activity may be through the deletion of a suppressor cell population acting on the NK cells.
Following the intraperitoneal injection of cis-diamino-dichloro-platinum (II) (CDDP) into tumor-bearing mice, two immune responses were augmented. The total splenic plaque-forming cells response to sheep red blood cells and the delayed-type hypersensitivity reaction to oxazolone were higher in treated animals than in the control groups. This observation may be relevant in the establishment of clinical protocols associating CDDP and other cytotoxic drugs.
Three new nitrosourea analogs (CNCC, RFCNU, and chlorozotocin) had comparable activities in vivo against L1210 leukemia cells. In addition to the antileukemia effect, these drugs also decreased both the humoral immune response to sheep red blood cells and the delayed hypersensitivity reaction to oxazolone. The immunodepression induced by these agents lasted at least 25 days, and could not be reversed by the transplantation of normal syngenic bone marrow cells into treated animals.
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