The polymeric immunoglobulin receptor: structure and synthesis

Kaetzel, Charlotte S.; Blanch, Vincent J.; Hempen, Paula M.; Phillips, Kimberly M.; Piskurich, Janet F.; Youngman, Kenneth R.

doi:10.1042/bst0250475

Cited by 42 publications

(23 citation statements)

References 11 publications

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“…Next, we investigated the role of two previously reported putative TNF-␣-responsive elements: an ISRE in exon 1 (26,27) and an NF-B/Rel site centered around position Ϫ450 in the upstream promoter (18,25). The former is 100% conserved between human, rat, and murine sequence, although the position relative to the transcriptional start site differs somewhat (Fig.…”

Section: An Isre In Exon 1 Is Required For Full Tnf-␣ Responsiveness mentioning

confidence: 99%

“…2, pSC28). Exon 1 of the pIgR/SC gene contains an ISRE involved in its IFN-␥ responsiveness (32), which has also been implicated in its TNF-␣ responsiveness (26,27). This exon 1 ISRE is 100% conserved among human, rat, and mouse (Fig.…”

Section: Mapping Of the Tnf-␣ Responsiveness Of The Human Pigr/sc Genmentioning

confidence: 99%

“…Both IFN-␥ and TNF-␣ have been demonstrated to induce production of IRF-1 in HT-29 cells (26,27,32), suggesting that this transcription factor participates in TNF-␣-mediated transcriptional activation of the pIgR/SC gene via binding to the exon 1 ISRE. The idea that NF-B might synergize with a member of the IRF family to regulate pIgR/SC expression is supported by the documented cooperation between these two transcription factor families in the regulation of the IFN-␤ gene (37,38).…”

Section: Mapping Of the Tnf-␣ Responsiveness Of The Human Pigr/sc Genmentioning

confidence: 99%

“…Piskurich et al (32) reported the presence of two other putative ISREs in the promoter region, centered around position Ϫ132 and Ϫ99, respectively, which bound constitutively expressed nuclear factors. Based on deletional analysis, they suggested the involvement of these two ISREs both in the IFN-␥-(32) and TNF-␣-mediated (26) up-regulation of human pIgR/SC. However, the direct involvement of either of these two ISREs has not yet been demonstrated by mutational analysis.…”

Section: Possible Role Of Other Transcription Factor Binding Sitesmentioning

confidence: 99%

“…3 and 24). TNF-␣-mediated transcriptional up-regulation of pIgR/SC was shown to depend on NF-B/Rel activation (25) and an IFN-stimulated response element (ISRE) located in exon 1 (26,27). However, the effect mediated by described DNA elements could not account for the degree of up-regulation indicated by the increased level of mRNA and by nuclear run-on experiments (18).…”

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confidence: 99%

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A Novel NF-κB/Rel Site in Intron 1 Cooperates with Proximal Promoter Elements to Mediate TNF-α-Induced Transcription of the Human Polymeric Ig Receptor

Schjerven

Brandtzæg

Johansen

2001

The Journal of Immunology

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Secretory Abs constitute the first line of specific immune defense at mucosal surfaces. Such Abs are generated by the active transport of polymeric Ig (pIg) across secretory epithelia mediated by the pIgR, also known as transmembrane secretory component (SC). The proinflammatory cytokine TNF-α is a key mediator of host responses to infections, and it can stimulate protein synthesis-dependent transcriptional up-regulation of pIgR/SC in the HT-29 intestinal adenocarcinoma cell line. By reporter gene assay we identified a novel TNF-α-responsive region located within a 748-bp fragment in intron 1 of the human pIgR/SC gene which depended on an NF-κB/Rel site for full responsiveness. EMSAs demonstrated preferential binding of the NF-κB/Rel family member p65 (RelA) to this DNA element after TNF-α stimulation, with weaker and more delayed binding of p50. Furthermore, the TNF-α-responsive region in intron 1 required cooperation with DNA elements located in the proximal promoter region of the gene. Mutational analysis demonstrated that an IFN-stimulated response element near the transcriptional start site in exon 1 was involved in the TNF-α responsiveness. Thus, DNA elements located >4 kb apart were found to cooperate in TNF-α-induced pIgR/SC up-regulation. The intronic TNF-α-responsive enhancer overlapped with a recently identified IL-4-responsive enhancer. Several intronic DNA elements found to be functionally important in the human gene are highly conserved between the human and mouse pIgR/SC genes, suggesting the presence of a conserved cytokine-responsive enhancer region.

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Section: An Isre In Exon 1 Is Required For Full Tnf-␣ Responsiveness mentioning

confidence: 99%

Section: Mapping Of the Tnf-␣ Responsiveness Of The Human Pigr/sc Genmentioning

confidence: 99%

Section: Mapping Of the Tnf-␣ Responsiveness Of The Human Pigr/sc Genmentioning

confidence: 99%

Section: Possible Role Of Other Transcription Factor Binding Sitesmentioning

confidence: 99%

mentioning

confidence: 99%

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A Novel NF-κB/Rel Site in Intron 1 Cooperates with Proximal Promoter Elements to Mediate TNF-α-Induced Transcription of the Human Polymeric Ig Receptor

Schjerven

Brandtzæg

Johansen

2001

The Journal of Immunology

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Different regulatory pathways employed in cytokine-enhanced expression of secretory component and epithelial HLA class I genes

et al. 1999

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The transmembrane secretory component (SC, or pIg receptor) plays a crucial role in mucosal immunity by translocating dimeric IgA and pentameric IgM through exocrine epithelia. This receptor is up-regulated by cytokines in parallel with increased epithelial HLA expression. By use of the human epithelial cell line HT-29m3, we show that IFN-+ , TNF- § and IL-4 activate transcription of the SC gene. This activation was slow, suggesting mediation via newly synthesized protein factors. IFN-+ and TNF- § , but not IL-4, also up-regulated expression of HLA class I genes. However, this gene induction was rapid and did not depend on new protein synthesis. Nuclear run-on experiments showed that the transcription rate of HLA class I genes nearly peaked after only 30 min of IFN-+ or TNF- § stimulation, whereas the SC transcription rate did not peak until after 20-36 h of IFN-+ , TNF- § or IL-4 stimulation. Gel electrophoresis mobility shift assays demonstrated binding of nuclear proteins from cytokine-stimulated HT-29 cells to consensus elements in the promoter of the SC gene, involving the binding site for the nuclear factor-O B p50 subunit after TNF- § stimulation, and IFN-stimulated response element after IFN-+ stimulation (and weakly after TNF- § ). Our observations in vitro likely parallel events in vivo by which activated mucosal T cells and macrophages enhance pIg receptor-mediated external transport of secretory IgA and IgM and up-regulate epithelial HLA expression.

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Mucosal Immune Defense

Kaetzel¹

Encyclopedic Reference of Cancer

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The polymeric immunoglobulin receptor: structure and synthesis

Cited by 42 publications

References 11 publications

A Novel NF-κB/Rel Site in Intron 1 Cooperates with Proximal Promoter Elements to Mediate TNF-α-Induced Transcription of the Human Polymeric Ig Receptor

A Novel NF-κB/Rel Site in Intron 1 Cooperates with Proximal Promoter Elements to Mediate TNF-α-Induced Transcription of the Human Polymeric Ig Receptor

Different regulatory pathways employed in cytokine-enhanced expression of secretory component and epithelial HLA class I genes

Mucosal Immune Defense

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