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Title 

Aryl hydrocarbon receptor-dependent inhibition of AP-1 activity by 2,3,7,8-tetrachlorodibenzo-p-dioxin in activated B cells

Authors 

J H SuhY J JeonHwan Mook KimJong Soon KangN E KaminskiKyu-Hwan Yang

Publisher 

Elsevier

Issue Date 

2002

Citation 

Toxicology and Applied Pharmacology, vol. 181, no. 2, pp. 116-123

Keywords 

AhRAP-1B cellTCDD2,2',5,5' tetrachlorobiphenyl2,3,7,8 tetrachlorodibenzo para dioxinalpha naphthoflavonearomatic hydrocarbon receptorbiphenyl derivativechloramphenicol acetyltransferase

Abstract 

B cells have been identified as sensitive cellular targets responsible for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-mediated suppression of humoral immunity. In previous studies, TCDD was shown to produce a significant inhibition of IgM secretion and mu gene expression in LPS-activated CH12.LX B cells (AhR expressing) but not in BCL-1 B cells (AhR deficient). The present studies extend these previous findings by investigating the effect of TCDD on AP-1 and nuclear factor (NF)-κB, both of which play an important role in B-cell activation, differentiation, and immunoglobulin (Ig) gene expression. Electrophoretic mobility shift assays and chloramphenicol acetyl transferase reporter gene experiments demonstrated that lipopolysaccharide (LPS)-induced DNA binding and transcriptional activity of AP-1 was markedly inhibited by TCDD at 24, 48, and 72 h after cellular activation of CH12.LX cells. Conversely, TCDD treatment produced no significant change on the activity of NF-κB. Two AhR antagonists, α-naphthoflavone and 2,2′,5,5′-tetrachlorobiphenyl, attenuated TCDD-induced inhibition of AP-1 binding in CH12.LX cells. Concordant with this result, TCDD did not inhibit LPS-induced AP-1 activity in BCL-1 B cells. Moreover, supershift analysis revealed the major component of the AP-1 complex in LPS-activated CH12.LX cells was c-Jun. Additional studies revealed that the nuclear c-jun and c-jun steady-state mRNA expression was inhibited by TCDD treatment. Collectively, these results suggest that TCDD-induced inhibition of IgM expression by B cells may be mediated, at least in part, through a down-regulation of AP-1 activity in an AhR-dependent manner.

ISSN 

0041-008X

Link 

http://dx.doi.org/10.1006/taap.2002.9403

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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