Silicosis is a chronic lung disease characterized by diffuse fibrosis in the lungs, primarily caused by continuous exposure to silica dust. The onset and progression of silicosis involve complex interactions between various immune cells and molecules, making it a poorly understood pathological process. Innate and adaptive immune cells, along with their cytokines, play significant roles in the development of silicosis. This review aims to describe the roles of immune cells and cytokines in silicosis and summarize current knowledge on inflammatory signaling pathways associated with the disease, providing insights into novel targets and strategies for treating silicosis-related inflammation. Key immune cells involved in silicosis include macrophages, neutrophils, mast cells, dendritic cells, and T/B lymphocytes. Macrophages, particularly alveolar macrophages (AMs), are central to the pathology of silicosis, regulating both inflammation and fibrosis. Neutrophils, recruited to the lungs in response to silica exposure, release neutrophil extracellular traps (NETs) and promote fibrosis. Mast cells, while less studied, are activated in silica-induced inflammation and regulate vascular permeability and fibroblast growth. Dendritic cells (DCs) modulate immune responses and contribute to the development of silicosis. Adaptive immune cells, including Th1, Th2, Th17, and regulatory T cells (Tregs), play crucial roles in the balance between inflammation and fibrosis. Pro-inflammatory cytokines such as IL-1β, IL-6, TNF-α, and TGF-β are key mediators in silicosis. IL-1β, a downstream product of NLRP3 inflammasome activation, promotes inflammation and fibrosis. IL-6, secreted by various cells, increases the risk of pulmonary fibrosis and modulates immune responses. TNF-α initiates inflammatory responses and stimulates TGF-β expression, promoting fibrosis. TGF-β, a fibrogenic mediator, promotes extracellular matrix (ECM) accumulation and inhibits matrix degradation. Growth factors like PDGF and CTGF also contribute to fibrosis. Inflammatory signaling pathways, including the NF-κB, MAPK, Fas/FasL, and cGAS-STING pathways, are involved in the pathogenesis of silicosis. These pathways regulate immune responses, cell proliferation, and fibrosis. For example, NF-κB activation in macrophages modulates apoptosis, while MAPK signaling pathways mediate fibroblast proliferation and ECM production. Biomarkers for early diagnosis of silicosis include inflammatory cytokines, inflammatory proteins (e.g., HO-1, HMGB1), the NLRP3 inflammasome, and DNA methylation. These biomarkers are present in cellular oxidative stress responses, immune responses, and tissue damage and repair processes. Treatment options for silicosis include lung lavage, transplantation,Silicosis is a chronic lung disease characterized by diffuse fibrosis in the lungs, primarily caused by continuous exposure to silica dust. The onset and progression of silicosis involve complex interactions between various immune cells and molecules, making it a poorly understood pathological process. Innate and adaptive immune cells, along with their cytokines, play significant roles in the development of silicosis. This review aims to describe the roles of immune cells and cytokines in silicosis and summarize current knowledge on inflammatory signaling pathways associated with the disease, providing insights into novel targets and strategies for treating silicosis-related inflammation. Key immune cells involved in silicosis include macrophages, neutrophils, mast cells, dendritic cells, and T/B lymphocytes. Macrophages, particularly alveolar macrophages (AMs), are central to the pathology of silicosis, regulating both inflammation and fibrosis. Neutrophils, recruited to the lungs in response to silica exposure, release neutrophil extracellular traps (NETs) and promote fibrosis. Mast cells, while less studied, are activated in silica-induced inflammation and regulate vascular permeability and fibroblast growth. Dendritic cells (DCs) modulate immune responses and contribute to the development of silicosis. Adaptive immune cells, including Th1, Th2, Th17, and regulatory T cells (Tregs), play crucial roles in the balance between inflammation and fibrosis. Pro-inflammatory cytokines such as IL-1β, IL-6, TNF-α, and TGF-β are key mediators in silicosis. IL-1β, a downstream product of NLRP3 inflammasome activation, promotes inflammation and fibrosis. IL-6, secreted by various cells, increases the risk of pulmonary fibrosis and modulates immune responses. TNF-α initiates inflammatory responses and stimulates TGF-β expression, promoting fibrosis. TGF-β, a fibrogenic mediator, promotes extracellular matrix (ECM) accumulation and inhibits matrix degradation. Growth factors like PDGF and CTGF also contribute to fibrosis. Inflammatory signaling pathways, including the NF-κB, MAPK, Fas/FasL, and cGAS-STING pathways, are involved in the pathogenesis of silicosis. These pathways regulate immune responses, cell proliferation, and fibrosis. For example, NF-κB activation in macrophages modulates apoptosis, while MAPK signaling pathways mediate fibroblast proliferation and ECM production. Biomarkers for early diagnosis of silicosis include inflammatory cytokines, inflammatory proteins (e.g., HO-1, HMGB1), the NLRP3 inflammasome, and DNA methylation. These biomarkers are present in cellular oxidative stress responses, immune responses, and tissue damage and repair processes. Treatment options for silicosis include lung lavage, transplantation,