Interferon-induced antiviral actions in Friend leukemia cells: Role of membrane gangliosides

The interactions between interferon (IFN) and membrane gangliosides have been analyzed in Friend leukemia cells (FLC). The GM1-cholera toxin (CT) model has been selected as a reference system for a high-affinity ganglioside-ligand binding. Two gangliosides have been detected in FLC extracts: a disialoganglioside (∼ 95%) and a monosialoganglioside (∼ 5%) which migrate respectively as GD1a and GM1. Unilammellar liposomes containing either mixed commercial gangliosides or GD1a or GM1 bind three to eight fold more IFN (both partially purified and pure) than gangliosides-free liposomes. Only 3-4% of the input IFN was bound, whereas GM1-containing liposomes bound almost 50% of [3H]acetyl-CT. Neuraminidase treatment of FLC, which converts GD1a-like into the GM1-like ganglioside, does not significantly modify the IFN-induced antiviral effects. CT binding to FLC as well as CT-induced elevation of endocellular cyclic AMP levels in FLC were instead markedly increased by the same neuraminidase treatment. Further, pretreatment of FLC with either GD1a or GM1 or gangliosides extracted from FLC did not change the IFN-induced establishment of the antiviral state. These data provide convincing evidence that FLC gangliosides do not represent the IFN high-affinity receptors nor specifically mediate IFN effects, even though they bind IFN to some extent. © 1982.