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Biochem Biophys Res Commun. 2008 Oct 24;375(3):331-5. doi: 10.1016/j.bbrc.2008.07.156. Epub 2008 Aug 9.

Aryl hydrocarbon receptor signaling mediates expression of indoleamine 2,3-dioxygenase.

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1
Department of Environmental Toxicology, University of California, One Shields Avenue, Davis, CA 95616, USA.

Abstract

Aryl hydrocarbon receptor (AhR) activation by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) leads to immune suppression associated with the induction of regulatory T cells (T(reg)) expressing the transcription factor Foxp3. The immunological mechanisms of suppression are not well understood however dendritic cells (DC) are considered a key target for AhR-mediated immune suppression. Here we show that activation of AhR by TCDD induces DC indoleamine 2,3-dioxygenase 1 (IDO1) and indoleamine 2,3-dioxygenase-like protein (IDO2). Induction of IDO1 and IDO2 was also found in lung and spleen associated with an increase of the T(reg) marker Foxp3 in spleen of TCDD-treated C57BL/6 mice, which is suppressed by inhibition of IDO. These data indicate that AhR-activation is an important signaling pathway for IDO expression and suggest a critical role of IDO in the mechanism leading to the generation of T(reg) that mediates the immune suppression through activation of AhR.

PMID:
18694728
PMCID:
PMC2583959
DOI:
10.1016/j.bbrc.2008.07.156
[Indexed for MEDLINE]
Free PMC Article
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