Inhibition of beta-interferon augmentation of murine natural killer cytotoxicity by gangliosides.
Interferons cause augmentation of natural killer (NK) cell activity, which might be a major reason for their antitumor effect. Antiviral and antigrowth effects of mouse beta interferon are inhibited by mono-, di-, and trisialogangliosides commonly found in brain extracts, but also in membranes of many other cells. Results presented in this report show that preincubation of mouse beta interferon with a brain ganglioside mixture or its isolated major components Gm1, Gd1a, Gd1b, and Gt1b (see Aberrations) prior to addition to effector spleen cells, inhibits NK-cell enhancement due to interferon in a dose-dependent manner. When spleen cells are treated with individual gangliosides alone, spontaneous NK cell activity is not affected. Pretreatment of effector cells with gangliosides prior to addition of interferon does not inhibit subsequent augmentation of NK cell activity by beta interferon. Also, target susceptibility remains unaltered in the presence of gangliosides. Thus the inhibitory effect of gangliosides appears to involve competition for interaction of beta interferon with the NK cells.
D000818:Animals; D003602:Cytotoxicity, Immunologic / Q000187:drug effects; D005732:Gangliosides / Q000494:pharmacology*; D066298:In Vitro Techniques; D007370:Interferon Type I / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D007694:Killer Cells, Natural / Q000187:drug effects* / Q000276:immunology; D051379:Mice; D008808:Mice, Inbred CBA
D005732:Gangliosides; D007370:Interferon Type I