Background: Occupational crystalline silica (CS) particle exposure leads to silicosis. The burden of CS-associated disease remains high, and treatment options are limited due to vague mechanisms. CD4 ⁺ tissue-resident memory T cells (T _RM) accumulate in the lung responded to CS particles, mediating the pathogenesis of silicosis. Methods: Based on silicosis murine model by single intratracheal instillation of CS suspension, we further employ adoptive transfer, FTY720 treatment, and parabiosis murine model to explore their source. After defining T _RM cell subsets by CD103 and CD69, we intervene CD103 ⁺subset and block IL-7 signaling to alleviate silicosis. Results: The CD4 ⁺ T _RM cells are derived from peripheral lymphocyte recruitment and in situ expansion. Specifically, T _RM-Treg cells depend more on circulating T cell replenishment. The cell retention markers CD103 and CD69 can divide the T _RM cells into effector and regulatory subsets. However, targeting CD103 ⁺ T _RM-Treg cells do not mitigate disease phenotype since the T _RM subsets exerted immunosuppressive but not pro-fibrotic roles. We further dissect that IL-7 signaling promotes the progression of silicosis by tuning the maintenance of T _RM-effector T cells. Conclusion: Our findings highlight the distinct role of CD4 ⁺ T _RM cells in mediating CS-induced fibrosis and provide potential therapeutic strategies for silicosis.