Abstract
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 T H2 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.
Original language | English (US) |
---|---|
Pages (from-to) | 245-247 |
Number of pages | 3 |
Journal | Science |
Volume | 269 |
Issue number | 5221 |
DOIs | |
State | Published - 1995 |
Externally published | Yes |
ASJC Scopus subject areas
- General