title: [Immune System Reaction against Environmental Pollutants].
abstract: Environmental pollutants (such as diesel exhaust particles and silica) cause disorders ranging from bronchial asthma to malignant tumors. In recent years, it has been reported that some of the signaling pathways in which environmental contaminants act in vivo are associated with innate immunity. Innate immunity recognizes ligands and induces inflammation. Those ligands are pathogen-associated molecular patterns (PAMPs: e.g., lipopolysaccharide) and danger-associated molecular patterns (DAMPs: e.g., cholesterol crystallization or uric acid crystal). Activation of innate immunity stimulates the acquired immunity system. Therefore, innate immunity regulates the strength of the general immune system. Furthermore, crystal silica, which is an environmental pollutant, activates innate immunity as a ligand. Innate immunity involves the membrane-bound Toll-like receptors (TLR) and cytoplasm-localized nucleotide-binding oligomerization domain (NOD)-like receptors (NLR). We reported the innate immunity-system-related diseases such as Crohn's disease, Blau syndrome, myelogenous leukemia, and sarcoidosis. An inflammasome complex containing NLR has attracted attention owing to its correlation with the onset of several diseases. It is reported that the inflammasome activation is related to the development of lifestyle-related diseases such as myocardial infarction and fatty liver. It is also reported that the mechanism by which crystal silica and asbestos cause inflammation involves the inflammasome activation. Analyzing the genes of innate immunity contributes to the clarification of the mechanism of disease onset caused by environmental pollutants.
authors.affiliation: Department of Public Health, Yamaguchi University Graduate School of Medicine.
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Tanabe
authors.forename: Natsu
authors.initials: N
authors.lastname: Yamaguchi
authors.forename: Masayuki
authors.initials: M
authors.lastname: Okuda
authors.forename: Yasutaka
authors.initials: Y
authors.lastname: Ishimaru
authors.forename: Hidekazu
authors.initials: H
authors.lastname: Takahashi
mesh_terms: D056704:Adaptive Immunity / Q000276:immunology; D048868:Adaptor Proteins, Signal Transducing / Q000276:immunology; D001194:Asbestos / Q000276:immunology; D003460:Crystallization; D004785:Environmental Pollutants / Q000276:immunology*; D006801:Humans; D007107:Immune System / Q000276:immunology*; D007113:Immunity, Innate / Q000235:genetics / Q000276:immunology*; D058847:Inflammasomes / Q000276:immunology; D000069452:Pathogen-Associated Molecular Pattern Molecules / Q000276:immunology; D018160:Receptors, Cytoplasmic and Nuclear / Q000276:immunology; D012822:Silicon Dioxide / Q000276:immunology; D051193:Toll-Like Receptors / Q000276:immunology
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D004785:Environmental Pollutants; D058847:Inflammasomes; D000069452:Pathogen-Associated Molecular Pattern Molecules; D018160:Receptors, Cytoplasmic and Nuclear; D051193:Toll-Like Receptors; D001194:Asbestos; D012822:Silicon Dioxide