Several groups have reported that Th1 mediators such as IFN-γ, interleukin(IL)-12, and chemokine(C-C motif) ligand 3 (CCL3) are present in the lungs of mice challenged with SR antigen [15,16], and that IFN-γ deficient mice are protected from developing HP [17]. This evidence concerns the gene IFNG and hypersensitivity pneumonitis.