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

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dc.contributor.authorJ H Suh-
dc.contributor.authorY J Jeon-
dc.contributor.authorHwan Mook Kim-
dc.contributor.authorJong Soon Kang-
dc.contributor.authorN E Kaminski-
dc.contributor.authorKyu-Hwan Yang-
dc.date.accessioned2017-04-19T08:59:19Z-
dc.date.available2017-04-19T08:59:19Z-
dc.date.issued2002-
dc.identifier.issn0041-008X-
dc.identifier.uri10.1006/taap.2002.9403ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/5939-
dc.description.abstractB 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.-
dc.publisherElsevier-
dc.titleAryl hydrocarbon receptor-dependent inhibition of AP-1 activity by 2,3,7,8-tetrachlorodibenzo-p-dioxin in activated B cells-
dc.title.alternativeAryl hydrocarbon receptor-dependent inhibition of AP-1 activity by 2,3,7,8-tetrachlorodibenzo-p-dioxin in activated B cells-
dc.typeArticle-
dc.citation.titleToxicology and Applied Pharmacology-
dc.citation.number2-
dc.citation.endPage123-
dc.citation.startPage116-
dc.citation.volume181-
dc.contributor.affiliatedAuthorHwan Mook Kim-
dc.contributor.affiliatedAuthorJong Soon Kang-
dc.contributor.affiliatedAuthorKyu-Hwan Yang-
dc.contributor.alternativeName서재홍-
dc.contributor.alternativeName전영진-
dc.contributor.alternativeName김환묵-
dc.contributor.alternativeName강종순-
dc.contributor.alternativeNameKaminski-
dc.contributor.alternativeName양규환-
dc.identifier.bibliographicCitationToxicology and Applied Pharmacology, vol. 181, no. 2, pp. 116-123-
dc.identifier.doi10.1006/taap.2002.9403-
dc.subject.keywordAhR-
dc.subject.keywordAP-1-
dc.subject.keywordB cell-
dc.subject.keywordTCDD-
dc.subject.localAhR-
dc.subject.localAP-1-
dc.subject.localB cell-
dc.subject.localB cells-
dc.subject.localTCDD-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > Laboratory Animal Resource & Research Center > 1. Journal Articles
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