Lack of Interferon γ Receptor β Chain and the Prevention of Interferon γ Signaling in T <sub>H</sub> 1 Cells
Alessandra B. Pernis(Columbia University), Sanjay Gupta(Columbia University), Kenneth J. Gollob(Merck Biopharma Co., Ltd. (Japan)), Evan S. Garfein(Columbia University), Robert L. Coffman(Merck Biopharma Co., Ltd. (Japan)), Chris Schindler(Columbia University), Paul B. Rothman(Columbia University)
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Abstract
The ability of interferon gamma (IFN-gamma) 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-gamma signaling pathway. The IFN-gamma-inducible signal transducing factor (STF-IFN gamma) was activated in murine TH2 but not in TH1 cell clones, because in the latter the second chain of the IFN-gamma receptor (accessory factor 1 or IFN-gamma R beta) was absent. Thus, TH1 cells use receptor modification to prevent the activation of STF-IFN gamma and achieve an IFN-gamma-resistant state.
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