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Vol. 53, Issue 4, 623-629, April 1998
Department of Pharmacology and Toxicology and Department of
Pathology, Michigan State University, East Lansing, Michigan 48824
The immune system has been identified as a sensitive target for the
toxic effects produced by
2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Furthermore,
the B cell has been identified as a sensitive cellular target of TCDD
by previous cell-type fractionation studies from this laboratory. The
mechanism responsible for the immunotoxic effects produced by TCDD is
unclear; however, many of the biological effects of TCDD are thought to
be mediated by the aryl hydrocarbon receptor (AhR). Here, we describe
two B cell lines that differ considerably in their expression of the
AhR and in their sensitivity to TCDD. Our results demonstrated a marked
expression of the AhR protein in the CH12.LX B cell line but not in the
BCL-1 B cell line. Transcripts for the AhR were not detected by reverse
transcriptase-polymerase chain reaction in the BCL-1 cells. The AhR
nuclear translocator (ARNT) protein was highly expressed in both cell
lines. In addition, the AhR and ARNT are functional in CH12.LX cells as
demonstrated by TCDD-induced CYP1A1 induction. TCDD did not induce
CYP1A1 in BCL-1 cells. Furthermore, TCDD treatment resulted in
suppression of lipopolysaccharide (LPS)-induced IgM secretion in
CH12.LX cells. Conversely, TCDD-induced inhibition of IgM secretion was
not demonstrated in LPS-stimulated BCL-1 cells, implicating a role for
the AhR in the inhibition of B cell effector function. LPS-induced
differentiation of the CH12.LX cells also resulted in a marked
induction of Ahr expression which was not induced in LPS-stimulated
BCL-1 cells. These studies have implicated the AhR as a critical factor
in TCDD-induced inhibition of IgM secretion and have demonstrated an
induction of AhR gene and protein expression after B cell activation.
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