Ligand-Induced Autoregulation of IFN-γ Receptor β Chain Expression in T Helper Cell Subsets

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Abstract
Interferon γ (IFN-γ) responsiveness in certain cells depends on the state of cellular differentiation or activation. Here an in vitro developmental system was used to show that IFN-γ produced during generation of the CD4+ T helper cell type 1 (TH1) subset extinguishes expression of the IFN-γ receptor β subunit, resulting in TH1 cells that are unresponsive to IFN-γ. This β chain loss also occurred in IFN-γ-treated TH2 cells and thus represents a specific response of CD4+ T cells to IFN-γ rather than a TH1-specific differentiation event. These results define a mechanism of cellular desensitization where a cytokine down-regulates expression of a receptor subunit required primarily for signaling and not ligand binding.