Silicosis is a progressive disease of the lungs triggered by inhalation of crystalline silica dust, characterized mainly by chronic lung inflammation and fibrosis with silicosis nodules. Epidemiological data show that the disease is highly prevalent in occupationally exposed populations, such as mining and building construction, and has become a major occupational health problem worldwide. The pathological process involves complex interactions between multiple cell types, including alveolar macrophages, epithelial cells and fibroblasts, with imbalances in the regulation of the adaptive immune system, particularly T lymphocytes, receiving much attention in recent years, and the mechanisms are not well understood. In this paper, we summarize the roles of CD4⁺ helper T cells and CD8⁺ cytotoxic T cells in silicosis, including the imbalance between different types of T cells (Th1/Th2/Th17/Treg subpopulations), the imbalance of cytokines secreted by the same type of T cells and the balance between their different cellular functions, which accelerate the development of silicosis, and the different specificity of this dynamic imbalance in different pathological stages. This dynamic imbalance presents different specificities at different pathological stages, and excessive immune disorders can lead to a variety of complications such as dyspnoea and autoimmune diseases. Therefore, maintaining the immune balance of pulmonary T-cells is essential for the prevention and treatment of silicosis. At the same time, clinical interventions are still limited to dust exposure control, glucocorticoid symptomatic treatment and end-stage lung transplantation, and there is a lack of specific therapies to address the pathogenic mechanisms. Novel therapeutic strategies based on T-cell subpopulation rebalancing have also shown potential value and may provide new therapeutic ideas for silicosis. Overall, this paper provides a systematic review of the dual regulatory mechanisms of T cells in silicosis and explores therapeutic perspectives for disease control through immune homeostasis reestablishment.