Immunopathogenesis of asbestosis, silicosis, and coal workers' pneumoconiosis.
From these discussions, it is apparent that immunologic aberrations occur in several inorganic dust diseases. Although the role of these immunologic mechanisms in disease pathogenesis remains speculative, recent studies demonstrating the regulation of fibroblast proliferation by macrophage and asbestos or silica interaction support a role for this cell type in the immunopathogenesis of disease. Future cellular and humoral investigations of the bronchoalveolar lavage in workers with pneumoconiosis may clarify the immunologic contributions in the development of fibrosis observed in these diseases.
D000974:Antibodies, Antinuclear / Q000032:analysis; D001195:Asbestosis / Q000209:etiology / Q000276:immunology*; D003167:Complement Activation; D006801:Humans; D008214:Lymphocytes / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D009504:Neutrophils / Q000276:immunology; D010587:Phagocytosis; D011009:Pneumoconiosis / Q000209:etiology / Q000276:immunology*; D012829:Silicosis / Q000209:etiology / Q000276:immunology*
D000974:Antibodies, Antinuclear