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Title: Cutting edge: activation of the aryl hydrocarbon receptor by 2,3,7,8-tetrachlorodibenzo-p-dioxin generates a population of CD4+ CD25+ cells with characteristics of regulatory T cells.

Authors: Funatake, Castle J; Marshall, Nikki B; Steppan, Linda B; Mourich, Dan V; Kerkvliet, Nancy I

Published In J Immunol, (2005 Oct 01)

Abstract: Activation of the aryl hydrocarbon receptor (AhR) by its most potent ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), leads to immune suppression in mice. Although the underlying mechanisms responsible for AhR-mediated immune suppression are not known, previous studies have shown that activation of the AhR must occur within the first 3 days of an immune response and that CD4+ T cells are primary targets. Using the B6-into-B6D2F1 model of an acute graft-vs-host response, we show that activation of AhR in donor T cells leads to the generation of a subpopulation of CD4+ T cells that expresses high levels of CD25, along with CD62L(low), CTLA-4, and glucocorticoid-induced TNFR. These donor-derived CD4+ CD25+ cells also display functional characteristics of regulatory T cells in vitro. These findings suggest a novel role for AhR in the induction of regulatory T cells and provide a new perspective on the mechanisms that underlie the profound immune suppression induced by exposure to TCDD.

PubMed ID: 16177056 Exiting the NIEHS site

MeSH Terms: Animals; Disease Models, Animal; Environmental Pollutants/pharmacology*; Gene Expression/drug effects; Graft vs Host Disease/metabolism; L-Selectin/biosynthesis; L-Selectin/genetics; Lymphocyte Activation/drug effects; Mice; Mice, Inbred C57BL; Mice, Knockout; Polychlorinated Dibenzodioxins/pharmacology*; Receptors, Aryl Hydrocarbon/deficiency; Receptors, Aryl Hydrocarbon/metabolism*; Receptors, Aryl Hydrocarbon/physiology; Receptors, Interleukin-2/biosynthesis*; Receptors, Interleukin-2/genetics; Spleen/cytology; Spleen/drug effects; Spleen/metabolism; T-Lymphocytes, Regulatory/immunology*

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