Suppression of NK-mediated natural resistance by interferon treatment of murine lymphomas.
The observation that interferon (IFN) can suppress the NK lytic sensitivity of murine lymphomas in vitro led us to examine the consequences of this treatment on tumor behavior in vivo. Preincubation in IFN suppressed natural resistance to two lymphomas in syngeneic DBA/2 and semisyngeneic BDF1 mice in a dose-dependent manner, measured by the retention of (131I)dUrd-labeled tumor. Poly I:C enhancement of NK-mediated natural resistance in the lung, liver, and peritoneal cavity was also abolished by IFN pretreatment. IFN was, however, ineffective in altering the elimination of the IFN-resistant L1210R lymphoma when compared to its IFN-sensitive variant, L1210S. In DBA/2 mice that were made NK-deficient by treatment with cyclophosphamide or rabbit anti-asialo GM1 antiserum, or in congenitally NK-deficient bg/bg strain mice, IFN-treated tumor and control tumor were rejected equally well. This indicated that the effects of IFN were dependent on the presence of NK cells in these mice, and suggests that the IFN suppressed the sensitivity of the lymphomas to NK cell-mediated host resistance.
D000818:Animals; D003602:Cytotoxicity, Immunologic / Q000187:drug effects; D007108:Immune Tolerance; D007113:Immunity, Innate / Q000187:drug effects; D007372:Interferons / Q000494:pharmacology*; D007694:Killer Cells, Natural / Q000276:immunology*; D007939:Leukemia L1210 / Q000235:genetics / Q000276:immunology / Q000628:therapy*; D008113:Liver Neoplasms / Q000235:genetics / Q000276:immunology / Q000628:therapy; D008175:Lung Neoplasms / Q000235:genetics / Q000276:immunology / Q000628:therapy; D008223:Lymphoma / Q000235:genetics / Q000276:immunology / Q000628:therapy*; D051379:Mice; D008811:Mice, Inbred DBA; D008817:Mice, Mutant Strains; D010534:Peritoneal Neoplasms / Q000276:immunology / Q000628:therapy; D013160:Splenic Neoplasms / Q000235:genetics / Q000276:immunology / Q000628:therapy
D007372:Interferons