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

Christoph F A Vogel, Samuel R. Goth, Bin Dong, Isaac N Pessah, Fumio Matsumura

Research output: Contribution to journalArticle

151 Scopus citations

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 (Treg) 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 Treg 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 Treg that mediates the immune suppression through activation of AhR.

Original languageEnglish (US)
Pages (from-to)331-335
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume375
Issue number3
DOIs
StatePublished - Oct 24 2008

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Keywords

  • AhR
  • CD86
  • DC-CK1
  • Foxp3
  • IDO
  • IL-8
  • TCDD

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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