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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 Cells¹

Castle J. Funatake^*, Nikki B. Marshall^,, Linda B. Steppan^*, Dan V. Mourich^, and Nancy I. Kerkvliet^2,*,

^* Department of Environmental and Molecular Toxicology, Department of Microbiology, and Environmental Health Sciences Center, Oregon State University, Corvallis, OR 97331; and AVI Biopharma, Corvallis, OR 97333

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.

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