further demonstrated that compared to BALB/c wild-type mice, T-bet gene (Th1 cell-specific transcription factor) deficient mice were unable to produce Th1 cytokines such as IFN-γ and were more susceptible to pulmonary fibrosis in bleomycin-induced pulmonary fibrosis mice (17); and further, in silicosis mice model it was found that Th1 cells could facilitate the lungs to undergo the clearance of silica particles through the secretion of IFN-γ and IL-2. Here, IL2 is linked to pulmonary fibrosis.