Silicosis is a chronic lung disease caused by long-term inhalation of silica particles, leading to diffuse fibrosis. It is a complex disease involving multiple immune cells and inflammatory pathways. Silicosis is a major occupational disease in developing countries, with significant morbidity and mortality. Innate and adaptive immune cells, along with their cytokines, play a critical role in its development. This review discusses the roles of immune cells and cytokines in silicosis, and summarizes current knowledge on inflammatory signaling pathways associated with the disease, aiming to provide novel targets and strategies for the treatment of silicosis-related inflammation. Silicosis is characterized by macrophage-dominated pulmonary alveolitis and restricted pulmonary function. It is classified into three types: chronic, accelerated, and acute, based on silica exposure. Silicosis is associated with other diseases such as lung cancer, pulmonary tuberculosis, and interstitial fibrosis, which negatively affect quality of life. Despite high incidence and mortality rates, treatment options for silicosis-associated lung damage are limited, and the pathomechanisms remain poorly understood. Inflammation-related mechanisms are considered to underlie most cases of silica-induced lung injury. Understanding silica-induced inflammation cascades and inflammation-fibrosis relationships is critical for understanding the pathophysiology of silicosis. Macrophages, neutrophils, mast cells, dendritic cells, and adaptive immune cells are involved in silicosis. Macrophages are the first line of defense against silica, and their dysfunction leads to inflammation and fibrosis. Neutrophils contribute to inflammation by secreting cytokines and neutrophil extracellular traps (NETs). Mast cells play a role in silicosis by recruiting and activating other immune cells. Dendritic cells modulate immune responses by activating T lymphocytes. Adaptive immune cells, including T and B cells, are involved in silicosis, with Th1/Th2 imbalance playing a regulatory role in the inflammatory phase. Th17 cells also contribute to lung inflammation and fibrosis. Tregs have dual functions in silicosis, with a detrimental role in the early stages and a protective role in the later stages. B cells also play a pro-fibrotic role in silicosis. Inflammatory factors such as IL-1β, IL-6, TGF-β, TNF-α, and PDGF promote silicosis. The NLRP3 inflammasome is involved in silicosis, with its activation leading to the production of pro-inflammatory cytokines. The cGAS-STING pathway is also involved in silicosis, with its activation leading to the production of type-I IFN and other inflammatory factors. Inflammatory biomarkers such as HO-1, HMGB1, and DNA methylation are involved in silicosis. These biomarkers are important for the diagnosis and treatment of silicosis. Treatment options for silicosis include lung lavSilicosis is a chronic lung disease caused by long-term inhalation of silica particles, leading to diffuse fibrosis. It is a complex disease involving multiple immune cells and inflammatory pathways. Silicosis is a major occupational disease in developing countries, with significant morbidity and mortality. Innate and adaptive immune cells, along with their cytokines, play a critical role in its development. This review discusses the roles of immune cells and cytokines in silicosis, and summarizes current knowledge on inflammatory signaling pathways associated with the disease, aiming to provide novel targets and strategies for the treatment of silicosis-related inflammation. Silicosis is characterized by macrophage-dominated pulmonary alveolitis and restricted pulmonary function. It is classified into three types: chronic, accelerated, and acute, based on silica exposure. Silicosis is associated with other diseases such as lung cancer, pulmonary tuberculosis, and interstitial fibrosis, which negatively affect quality of life. Despite high incidence and mortality rates, treatment options for silicosis-associated lung damage are limited, and the pathomechanisms remain poorly understood. Inflammation-related mechanisms are considered to underlie most cases of silica-induced lung injury. Understanding silica-induced inflammation cascades and inflammation-fibrosis relationships is critical for understanding the pathophysiology of silicosis. Macrophages, neutrophils, mast cells, dendritic cells, and adaptive immune cells are involved in silicosis. Macrophages are the first line of defense against silica, and their dysfunction leads to inflammation and fibrosis. Neutrophils contribute to inflammation by secreting cytokines and neutrophil extracellular traps (NETs). Mast cells play a role in silicosis by recruiting and activating other immune cells. Dendritic cells modulate immune responses by activating T lymphocytes. Adaptive immune cells, including T and B cells, are involved in silicosis, with Th1/Th2 imbalance playing a regulatory role in the inflammatory phase. Th17 cells also contribute to lung inflammation and fibrosis. Tregs have dual functions in silicosis, with a detrimental role in the early stages and a protective role in the later stages. B cells also play a pro-fibrotic role in silicosis. Inflammatory factors such as IL-1β, IL-6, TGF-β, TNF-α, and PDGF promote silicosis. The NLRP3 inflammasome is involved in silicosis, with its activation leading to the production of pro-inflammatory cytokines. The cGAS-STING pathway is also involved in silicosis, with its activation leading to the production of type-I IFN and other inflammatory factors. Inflammatory biomarkers such as HO-1, HMGB1, and DNA methylation are involved in silicosis. These biomarkers are important for the diagnosis and treatment of silicosis. Treatment options for silicosis include lung lav