PMID- 18694728
OWN - NLM
STAT- MEDLINE
DCOM- 20080929
LR  - 20211020
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Print)
IS  - 0006-291X (Linking)
VI  - 375
IP  - 3
DP  - 2008 Oct 24
TI  - Aryl hydrocarbon receptor signaling mediates expression of indoleamine 
      2,3-dioxygenase.
PG  - 331-5
LID - 10.1016/j.bbrc.2008.07.156 [doi]
AB  - 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.
FAU - Vogel, Christoph F A
AU  - Vogel CF
AD  - Department of Environmental Toxicology, University of California, One Shields 
      Avenue, Davis, CA 95616, USA.
FAU - Goth, Samuel R
AU  - Goth SR
FAU - Dong, Bin
AU  - Dong B
FAU - Pessah, Isaac N
AU  - Pessah IN
FAU - Matsumura, Fumio
AU  - Matsumura F
LA  - eng
GR  - R01 ES005233-14/ES/NIEHS NIH HHS/United States
GR  - R01 ES005233/ES/NIEHS NIH HHS/United States
GR  - R21 ES015846-01A2/ES/NIEHS NIH HHS/United States
GR  - R21 ES015846/ES/NIEHS NIH HHS/United States
GR  - R01 ES019898/ES/NIEHS NIH HHS/United States
GR  - R21 ES015846-02/ES/NIEHS NIH HHS/United States
GR  - P01 ES011269/ES/NIEHS NIH HHS/United States
GR  - R01-ES05233/ES/NIEHS NIH HHS/United States
GR  - P01 ES011269-08/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20080809
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Indoleamine-Pyrrole 2,3,-Dioxygenase)
RN  - 0 (Polychlorinated Dibenzodioxins)
RN  - 0 (Receptors, Aryl Hydrocarbon)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Animals
MH  - *Immune Tolerance
MH  - Indoleamine-Pyrrole 2,3,-Dioxygenase/*metabolism
MH  - Interferon-gamma/pharmacology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Polychlorinated Dibenzodioxins/pharmacology
MH  - Receptors, Aryl Hydrocarbon/agonists/*metabolism
MH  - Signal Transduction
MH  - T-Lymphocytes, Regulatory/drug effects/enzymology/*immunology
PMC - PMC2583959
MID - NIHMS70652
EDAT- 2008/08/13 09:00
MHDA- 2008/09/30 09:00
PMCR- 2009/10/24
CRDT- 2008/08/13 09:00
PHST- 2008/06/28 00:00 [received]
PHST- 2008/07/30 00:00 [accepted]
PHST- 2008/08/13 09:00 [pubmed]
PHST- 2008/09/30 09:00 [medline]
PHST- 2008/08/13 09:00 [entrez]
PHST- 2009/10/24 00:00 [pmc-release]
AID - S0006-291X(08)01495-2 [pii]
AID - 10.1016/j.bbrc.2008.07.156 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2008 Oct 24;375(3):331-5. doi: 
      10.1016/j.bbrc.2008.07.156. Epub 2008 Aug 9.