[Chemical contamination of the environment and development of allergic and autoimmune diseases].
Chemical contamination of the environment is a considerably serious problem. At present, many environmental factors are responsible for the increase in the number of allergic and autoimmune diseases, and we hypothesize that this increase is caused by the widespread chemical contamination of the environment. Here, we focus on two chemicals, tributyltin (TBT), an environmental endocrine disrupter, and tetrachlorodibenzodioxin (TCDD), a highly toxic compound. TBT shifts the Th1/Th2 balance to Th2 through reduced IL-12 production by dendritic cells and augmentation of IL-10 production by B cells, indicating that TBT contributes to the increase in the number of allergic diseases. Furthermore, environmental factors are believed to contribute to the increased prevalence of autoimmune diseases, many of which are due to the activity of Th17 cells, a new helper T-cell subset characterized by IL-17 production. On the other hand, the aryl hydrocarbon receptor (AhR) acts as a ligand for mediating TCDD toxicity, and its expression is reportedly restricted to the Th17 cell subset in the CD4+T-cell lineage of mice. AhR activation during induction of experimental autoimmune encephalomyelitis causes accelerated onset and increased pathology in wild-type mice but not in AhR-deficient mice. AhR ligands may therefore represent co-factors in the development of autoimmune diseases. Although analysis of environmental factors that play a causative role in allergic and autoimmune diseases remains complex, it is thought that accumulation of relevant knowledge is necessary, as well as dissemination of information on environmental issues, particularly chemical contamination that causes disease.
Department of Dermatology, School of Medicine, Yokohama City University.
Kazuo
K
Takahashi
D000818:Animals; D001327:Autoimmune Diseases / Q000139:chemically induced*; D052244:Endocrine Disruptors / Q000633:toxicity*; D004785:Environmental Pollutants / Q000009:adverse effects*; D006801:Humans; D006967:Hypersensitivity / Q000209:etiology*; D000072317:Polychlorinated Dibenzodioxins / Q000633:toxicity*; D014220:Trialkyltin Compounds / Q000633:toxicity*
D052244:Endocrine Disruptors; D004785:Environmental Pollutants; D000072317:Polychlorinated Dibenzodioxins; D014220:Trialkyltin Compounds; C011559:tributyltin