Influenza infection stimulated IFN type I (IFNαβ) release to comparable levels in lungs of mice (data not shown) that possessed or lacked intact IFNγ receptor genes, but IFNαβ did not induce lung stromal cells to express IDO, suggesting that these cells are unresponsive to signals from IFNαβ. The gene discussed is IDO1; the disease is influenza.