|dc.contributor.author||J H Suh||-|
|dc.contributor.author||Y J Jeon||-|
|dc.contributor.author||Hwan Mook Kim||-|
|dc.contributor.author||Jong Soon Kang||-|
|dc.contributor.author||N E Kaminski||-|
|dc.description.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.||-|
|dc.title||Aryl hydrocarbon receptor-dependent inhibition of AP-1 activity by 2,3,7,8-tetrachlorodibenzo-p-dioxin in activated B cells||-|
|dc.title.alternative||Aryl hydrocarbon receptor-dependent inhibition of AP-1 activity by 2,3,7,8-tetrachlorodibenzo-p-dioxin in activated B cells||-|
|dc.citation.title||Toxicology and Applied Pharmacology||-|
|dc.contributor.affiliatedAuthor||Hwan Mook Kim||-|
|dc.contributor.affiliatedAuthor||Jong Soon Kang||-|
|dc.identifier.bibliographicCitation||Toxicology and Applied Pharmacology, vol. 181, no. 2, pp. 116-123||-|
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