Exposure to crystalline silica (CS) results in a persistent pulmonary inflammatory response, which results in abnormal tissue repair and excessive matrix deposition. Due to vague pathogenesis, there is virtually no practical therapeutic approach. Here we showed the pharmacological effects of TUDCA on CS-induced pulmonary inflammation and fibrosis. It also helped a faster recovery of CS-impaired pulmonary function. Mechanistically, TUDCA suppressed interferon (IFN)-γ and interleukin (IL)-17A productions by pulmonary helper T (Th) cells. We demonstrated that CS-boosted cytokine-producing Th cells were effector memory (T _EM ) phenotype. TUDCA decreased the pathogenic T _EM cells expansion in the lung. Using in vivo labeling method, we discovered the T _EM cells were lung tissue residency with CD103 expression. TUDCA’s anti-fibrotic effects were linked to decreasing IFN-γ producing CD103 ^- T _EM -like and IL-17A producing CD103 ⁺ T _RM -like T cells as well as restricting T _RM -like Treg cells in the lung. Specifically, TUDCA could restrain CD103 ⁺ T _RM -like Treg cell proliferation but not limit the CD103 ^- ones. Further characterization study proved that though the Tregs originally came from the thymus, the expressing levels of ST-2 were different, which provides insights into TUDCA’s various effects on cell proliferation. Collectively, our data paved the way to understanding the pathogenesis of silicosis and may provide new treatments for this pulmonary fibrotic disease.