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Molecular Pharmacology

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Research ArticleArticle

Aryl Hydrocarbon Receptor-Dependent Suppression by 2,3,7,8-Tetrachlorodibenzo-p-dioxin of IgM Secretion in Activated B Cells

Courtney E. W. Sulentic, Michael P. Holsapple and Norbert E. Kaminski
Molecular Pharmacology April 1998, 53 (4) 623-629; DOI: https://doi.org/10.1124/mol.53.4.623
Courtney E. W. Sulentic
Department of Pharmacology and Toxicology and Department of Pathology, Michigan State University, East Lansing, Michigan 48824
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Michael P. Holsapple
Department of Pharmacology and Toxicology and Department of Pathology, Michigan State University, East Lansing, Michigan 48824
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Norbert E. Kaminski
Department of Pharmacology and Toxicology and Department of Pathology, Michigan State University, East Lansing, Michigan 48824
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Abstract

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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Molecular Pharmacology: 53 (4)
Molecular Pharmacology
Vol. 53, Issue 4
1 Apr 1998
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Research ArticleArticle

Aryl Hydrocarbon Receptor-Dependent Suppression by 2,3,7,8-Tetrachlorodibenzo-p-dioxin of IgM Secretion in Activated B Cells

Courtney E. W. Sulentic, Michael P. Holsapple and Norbert E. Kaminski
Molecular Pharmacology April 1, 1998, 53 (4) 623-629; DOI: https://doi.org/10.1124/mol.53.4.623

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Research ArticleArticle

Aryl Hydrocarbon Receptor-Dependent Suppression by 2,3,7,8-Tetrachlorodibenzo-p-dioxin of IgM Secretion in Activated B Cells

Courtney E. W. Sulentic, Michael P. Holsapple and Norbert E. Kaminski
Molecular Pharmacology April 1, 1998, 53 (4) 623-629; DOI: https://doi.org/10.1124/mol.53.4.623
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