Host: The Japanese Society of Toxicology
Name : The 49th Annual Meeting of the Japanese Society of Toxicology
Date : June 30, 2022 - July 02, 2022
Both of exposure to crystalline silica and asbestos cause pneumoconiosis as well as lung cancer. However, the former is associated with autoimmune diseases like scleroderma, whereas the latter causes malignant mesothelioma. Inhaled those reach lung tissue, causing inflammation mediated by alveolar macrophages, but are also accumulated in lymph nodes, thought to contribute to a reason for related diseases. Therefore, our studies noted immunological effects of silica and asbestos and have conducted basic examinations with cell cultures and immunological analyses for peripheral blood specimens from patients. It has been clarified that both of lymphocytes exposed to silica and derived from silicosis showed activation and decreased suppressive function, whereas decreased anti-tumor immunity and increased suppressive function were seen in asbestos-exposed lymphocytes as well as those from mesothelioma. Silica exposure caused CD69+ activated cells and decreased Foxp3+ regulatory T (Treg) cells, and silicosis showed increased soluble IL-2R as activation marker and decreased Treg function in blood. In contrast, asbestos exposure caused decreased activating receptor on NK cells, Th1 function of CD4+ T cells and cytotoxicity of CD8+ T cells as well as increased Treg function, and mesothelioma also showed altered expression of marker molecules indicating decreased anti-tumor immunity. Those findings indicate that exposure to silica and asbestos not only causes inflammatory response in the bronchial alveoli, but also raise immune-functional effects of activation or suppression, leading to related autoimmune or malignant diseases respectively.
