Key result
Interferon-resistant Daudi clones lack initial IFN-alpha binding peaks, suggesting defective receptor activation.
The phenotype of IFN resistance in DIF8 and DIF9 cells may be related to a defect in receptor activation, while resistance in DIF3 cells appears unrelated to IFN binding.
Defect in receptor activation may explain resistance in DIF8/DIF9 clones; leaves open distinct mechanisms in DIF3 and clinical translation.
Three clones of Daudi cells, DIF3, DIF8 and DIF9, have been isolated which possess specific interferon (IFN) receptors even though these cells are resistant to both the antiviral and antiproliferative actions of human IFN-alpha. Studies with 125I-labelled cloned human IFN-alpha subspecies showed that clone DIF3 bound IFN in a manner identical to that of the IFN-sensitive parental cells. The initial peak of binding observed 30 min after treatment of either Daudi or DIF3 cells at 37 degrees C with IFN-alpha 2 or IFN-alpha 8 was, however, either absent or much reduced when using DIF8 cells which are resistant to the antiproliferative action of IFN-alpha 2 and -alpha 8. Similarly, no initial peak of binding was observed after treatment of DIF9 cells with IFN-alpha 2 at 37 degrees C. In accord with its reduced biological activity, the binding of 125I-IFN-alpha 1 to either Daudi or DIF8 cells was considerably lower than that of either of the other two IFN-alpha subspecies and followed the form of a hyperbola without an initial transitory peak of binding. It is suggested that the phenotype of IFN resistance of DIF8 and DIF9 cells may be related to a defect in receptor activation whereas the same phenotype of DIF3 cells would appear to be unrelated to IFN binding.
No takes yet. Share an insight, caveat, or question.
Dron et al. (1986) studied Interferon resistance in Daudi cells. Human IFN-alpha subspecies vs. IFN-sensitive parental Daudi cells was evaluated on Binding of 125I-labelled cloned human IFN-alpha subspecies. Interferon-resistant Daudi cell clones DIF8 and DIF9 lacked the initial peak of IFN-alpha binding seen in sensitive parental cells, suggesting a defect in receptor activation.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: