Lack of Interferon γ Receptor β Chain and the Prevention of Interferon γ Signaling in TH1 Cells
Science, 1995•science.org
The ability of interferon γ (IFN-γ) to inhibit the proliferation of type 2 T helper cells (TH2), but
not that of type 1 (TH1) cells, suggests that helper cell subsets might differ in their activation
of the IFN-γ signaling pathway. The IFN-γ-inducible signal transducing factor (STF-IFNγ) was
activated in murine TH2 but not in TH1 cell clones, because in the latter the second chain of
the IFN-γ receptor (accessory factor 1 or IFN-γRβ) was absent. Thus, TH1 cells use receptor
modification to prevent the activation of STF-IFNγ and achieve an IFN-γ-resistant state.
not that of type 1 (TH1) cells, suggests that helper cell subsets might differ in their activation
of the IFN-γ signaling pathway. The IFN-γ-inducible signal transducing factor (STF-IFNγ) was
activated in murine TH2 but not in TH1 cell clones, because in the latter the second chain of
the IFN-γ receptor (accessory factor 1 or IFN-γRβ) was absent. Thus, TH1 cells use receptor
modification to prevent the activation of STF-IFNγ and achieve an IFN-γ-resistant state.
The ability of interferon γ (IFN-γ) to inhibit the proliferation of type 2 T helper cells (TH2), but not that of type 1 (TH1) cells, suggests that helper cell subsets might differ in their activation of the IFN-γ signaling pathway. The IFN-γ-inducible signal transducing factor (STF-IFNγ) was activated in murine TH2 but not in TH1 cell clones, because in the latter the second chain of the IFN-γ receptor (accessory factor 1 or IFN-γRβ) was absent. Thus, TH1 cells use receptor modification to prevent the activation of STF-IFNγ and achieve an IFN-γ-resistant state.
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