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Vol. 52, Issue 6, 921-927, 1997
Department of Pharmacology and Toxicology and Department of
Pathology, Michigan State University, East Lansing, Michigan 48824 (R.B.C., N.E.K.) and
Dow Chemical Company, Toxicology Research
Laboratory, Midland, Michigan 48674 (M.P.H.)
The aryl hydrocarbon receptor (AhR) functions as a transcription factor
after ligand binding by halogenated aromatic hydrocarbons. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the most
toxic halogenated aromatic hydrocarbon, is dependent on binding to the
AhR to mediate a broad range of toxic effects. Immune suppression is
one of the most sensitive sequela associated with TCDD exposure, yet,
paradoxically, resting leukocytes express a relatively low amount of
AhR. Here we report that activation of leukocytes produced a 6-fold
increase in AhR steady state mRNA levels and a concordant increase in
AhR protein expression. Furthermore, leukocyte activation induced AhR
translocation, DNA binding to a dioxin response element, and CYP1A1
transcription in the absence of TCDD. Activated leukocytes exhibited an
even greater enhancement of dioxin response element binding by the AhR
in the presence of TCDD than in the absence of TCDD. These studies
suggest that the mechanism responsible for the sensitivity of
immunocompetent cells to TCDD may be directly associated with a marked
increase in AhR expression, which accompanies leukocyte activation.
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