IFN-γ treatment increases insulin binding and MHC class I expression in erythroleukemia cells

M Ferm, A Groünberg, M Tally - Immunological investigations, 1996 - Taylor & Francis
M Ferm, A Groünberg, M Tally
Immunological investigations, 1996Taylor & Francis
We have investigated if interferon-γ (IFN-γ) treatment of human K562 tumor cells, which
upregulates the expression of MHC class I antigens (MHC-I), simultaneously would
influence insulin binding. Treatment of K562 cells with recombinant human IFN-γ for 48 h
caused a significant increase of insulin binding at 37° C. Recombinant human tumor
necrosis factor-α (TNF-α) alone had no effect but acted synergistically with IFN-γ, leading to
a two-fold increase of insulin binding. No change in affinity, number of binding sites or cell …
We have investigated if interferon-γ (IFN-γ) treatment of human K562 tumor cells, which upregulates the expression of MHC class I antigens (MHC-I), simultaneously would influence insulin binding. Treatment of K562 cells with recombinant human IFN-γ for 48 h caused a significant increase of insulin binding at 37°C. Recombinant human tumor necrosis factor-α (TNF-α) alone had no effect but acted synergistically with IFN-γ, leading to a two-fold increase of insulin binding. No change in affinity, number of binding sites or cell surface expression of insulin receptors (IR) after IFN-γ treatment could be detected. The increased insulin binding observed at 37°C was not seen at 4°C, suggesting alteration of insulin internalization. The dose-response curve, as well as the time curve, for the increase in insulin binding after IFN-γ treatment correlated with enhanced cell surface expression of MHC-I antigens. However, the correlation was not absolute. Our results show that IFN-γ treatment alone or together with TNF-α, can alter the insulin binding to K562 cells without changing the expression or affinity of the IR. This correlates with the effect of IFN-γ on MHC-I expression. These results support the findings that MHC-I molecules associate and interact with the IR at the cell surface.
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