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Vol. 295, Issue 2, 705-716, November 2000
Department of Pharmacology and Toxicology and the National Center
for Food Safety and Toxicology, Michigan State University, East
Lansing, Michigan (C.E.W.S., N.E.K.); and Dow Chemical Company,
Midland, Michigan (M.P.H.)
The B-cell, a major cellular component of humoral immunity, has been
identified as a sensitive target of
2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The actual
molecular mechanism responsible for the immunotoxic effects produced by
TCDD is unclear; however, many of the biological effects produced by
TCDD are thought to be mediated by the aryl hydrocarbon receptor (AhR).
Using the CH12.LX B-cell line, the present studies show that inhibition
of µ gene expression and IgM protein secretion by polychlorinated
dibenzo-p-dioxin congeners follow a
structure-activity relationship for AhR binding. Furthermore, these
effects may be mediated by the two dioxin-responsive enhancer (DRE)-like sites that were identified within the Ig heavy chain 3'
-enhancer. Electrophoretic mobility shift assay-Western analysis demonstrated TCDD-induced binding of the AhR nuclear complex to both
DRE-like sites as well as TCDD-induced binding of several nuclear
factor-
B/Rel proteins to a B site, which overlaps one of the
DRE-like sites. Interestingly, B binding in the AhR-deficient BCL-1
B-cells was also induced by TCDD, demonstrating an AhR-independent effect of TCDD on B binding. Taken together, these results support an AhR/DRE-mediated mechanism for TCDD-induced inhibition of IgM expression.
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