Interleukin-17 deficient mice were thus spared radiation-induced lung disease, as evidenced by the absence of a distress response and by minimal histological changes in response to a radiation dose which produced pneumonitis with fibrosis in C57BL/6J mice and earlier onset respiratory distress with enhanced fibrosis in Tlr2/4−/− mice. The gene discussed is TLR2; the disease is lung disorder.