Endoplasmic reticulum stress-induced transcription factor, CHOP, is crucial for dendritic cell IL-23 expression
The endoplasmic reticulum (ER) stress response detects malfunctions in cellular physiology, and microbial pattern recognition receptors recognize external threats posed by infectious agents. This study has investigated whether proinflammatory cytokine expression by monocyte-derived dendritic cells i...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2010-10, Vol.107 (41), p.17698-17703 |
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| container_title | Proceedings of the National Academy of Sciences - PNAS |
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| creator | Goodall, Jane C. Wu, Changxin Zhang, Yongsheng McNeill, Louise Ellis, Lou Saudek, Vladimir Gaston, J. S. Hill |
| description | The endoplasmic reticulum (ER) stress response detects malfunctions in cellular physiology, and microbial pattern recognition receptors recognize external threats posed by infectious agents. This study has investigated whether proinflammatory cytokine expression by monocyte-derived dendritic cells is affected by the induction of ER stress. Activation of ER stress, in combination with Toll-like receptor (TLR) agonists, markedly enhanced expression of mRNA of the unique p19 subunit of IL-23, and also significantly augmented secretion of IL-23 protein. These effects were not seen for IL-12 secretion. The IL-23 gene was found to be a target of the ER stress-induced transcription factor C/EBP homologous protein (CHOP), which exhibited enhanced binding in the context of both ER stress and TLR stimulation. Knockdown of CHOP in U937 cells significantly reduced the synergistic effects of TLR and ER stress on IL-23p19 expression, but did not affect expression of other LPS-responsive genes. The integration of ER stress signals and the requirement for CHOP in the induction of IL-23 responses was also investigated in a physiological setting: infection of myeloid cells with Chlamydia trachomatis resulted in the expression of CHOP mRNA and induced the binding of CHOP to the IL-23 promoter. Furthermore, knockdown of CHOP significantly reduced the expression of IL-23 in response to this intracellular bacterium. Therefore, the effects of pathogens and other environmental factors on ER stress can profoundly affect the nature of innate and adaptive immune responses. |
| doi_str_mv | 10.1073/pnas.1011736107 |
| format | Article |
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S. Hill</creator><creatorcontrib>Goodall, Jane C. ; Wu, Changxin ; Zhang, Yongsheng ; McNeill, Louise ; Ellis, Lou ; Saudek, Vladimir ; Gaston, J. S. Hill</creatorcontrib><description>The endoplasmic reticulum (ER) stress response detects malfunctions in cellular physiology, and microbial pattern recognition receptors recognize external threats posed by infectious agents. This study has investigated whether proinflammatory cytokine expression by monocyte-derived dendritic cells is affected by the induction of ER stress. Activation of ER stress, in combination with Toll-like receptor (TLR) agonists, markedly enhanced expression of mRNA of the unique p19 subunit of IL-23, and also significantly augmented secretion of IL-23 protein. These effects were not seen for IL-12 secretion. The IL-23 gene was found to be a target of the ER stress-induced transcription factor C/EBP homologous protein (CHOP), which exhibited enhanced binding in the context of both ER stress and TLR stimulation. Knockdown of CHOP in U937 cells significantly reduced the synergistic effects of TLR and ER stress on IL-23p19 expression, but did not affect expression of other LPS-responsive genes. The integration of ER stress signals and the requirement for CHOP in the induction of IL-23 responses was also investigated in a physiological setting: infection of myeloid cells with Chlamydia trachomatis resulted in the expression of CHOP mRNA and induced the binding of CHOP to the IL-23 promoter. Furthermore, knockdown of CHOP significantly reduced the expression of IL-23 in response to this intracellular bacterium. Therefore, the effects of pathogens and other environmental factors on ER stress can profoundly affect the nature of innate and adaptive immune responses.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.1011736107</identifier><identifier>PMID: 20876114</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Agonists ; Binding sites ; Biological Sciences ; CCAAT/enhancer-binding protein ; Cell Line, Tumor ; Cells ; Chlamydia Infections - immunology ; Chlamydia trachomatis ; Chromatin Immunoprecipitation ; Cytokines ; Dendritic cells ; Dendritic Cells - immunology ; Endoplasmic reticulum ; Endoplasmic Reticulum - immunology ; Endoplasmic Reticulum - metabolism ; Environmental factors ; Enzyme-Linked Immunosorbent Assay ; Gene expression ; Gene Expression Regulation - immunology ; Genes ; Humans ; Immune response ; Immune system ; Infection ; Infections ; Inflammation ; Integration ; Interleukin 12 ; Interleukin 23 ; Interleukin-23 - immunology ; Interleukin-23 - metabolism ; Messenger RNA ; Monocytes ; Myeloid cells ; Oligonucleotide Array Sequence Analysis ; Pathogens ; Pattern recognition ; Promoters ; Proteins ; Ribonucleic acid ; RNA ; Secretion ; Stress ; Stress, Physiological - immunology ; Toll-like receptors ; Transcription Factor CHOP - metabolism ; Transcription factors</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2010-10, Vol.107 (41), p.17698-17703</ispartof><rights>Copyright National Academy of Sciences Oct 12, 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c597t-8fc4fa4c97bf342fb97f712695fd08aa724db3d5f7e614ac8b9aa502e97f21d13</citedby><cites>FETCH-LOGICAL-c597t-8fc4fa4c97bf342fb97f712695fd08aa724db3d5f7e614ac8b9aa502e97f21d13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/107/41.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/20780521$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/20780521$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,727,780,784,803,885,27924,27925,53791,53793,58017,58250</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20876114$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Goodall, Jane C.</creatorcontrib><creatorcontrib>Wu, Changxin</creatorcontrib><creatorcontrib>Zhang, Yongsheng</creatorcontrib><creatorcontrib>McNeill, Louise</creatorcontrib><creatorcontrib>Ellis, Lou</creatorcontrib><creatorcontrib>Saudek, Vladimir</creatorcontrib><creatorcontrib>Gaston, J. S. Hill</creatorcontrib><title>Endoplasmic reticulum stress-induced transcription factor, CHOP, is crucial for dendritic cell IL-23 expression</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>The endoplasmic reticulum (ER) stress response detects malfunctions in cellular physiology, and microbial pattern recognition receptors recognize external threats posed by infectious agents. This study has investigated whether proinflammatory cytokine expression by monocyte-derived dendritic cells is affected by the induction of ER stress. Activation of ER stress, in combination with Toll-like receptor (TLR) agonists, markedly enhanced expression of mRNA of the unique p19 subunit of IL-23, and also significantly augmented secretion of IL-23 protein. These effects were not seen for IL-12 secretion. The IL-23 gene was found to be a target of the ER stress-induced transcription factor C/EBP homologous protein (CHOP), which exhibited enhanced binding in the context of both ER stress and TLR stimulation. Knockdown of CHOP in U937 cells significantly reduced the synergistic effects of TLR and ER stress on IL-23p19 expression, but did not affect expression of other LPS-responsive genes. The integration of ER stress signals and the requirement for CHOP in the induction of IL-23 responses was also investigated in a physiological setting: infection of myeloid cells with Chlamydia trachomatis resulted in the expression of CHOP mRNA and induced the binding of CHOP to the IL-23 promoter. Furthermore, knockdown of CHOP significantly reduced the expression of IL-23 in response to this intracellular bacterium. Therefore, the effects of pathogens and other environmental factors on ER stress can profoundly affect the nature of innate and adaptive immune responses.</description><subject>Agonists</subject><subject>Binding sites</subject><subject>Biological Sciences</subject><subject>CCAAT/enhancer-binding protein</subject><subject>Cell Line, Tumor</subject><subject>Cells</subject><subject>Chlamydia Infections - immunology</subject><subject>Chlamydia trachomatis</subject><subject>Chromatin Immunoprecipitation</subject><subject>Cytokines</subject><subject>Dendritic cells</subject><subject>Dendritic Cells - immunology</subject><subject>Endoplasmic reticulum</subject><subject>Endoplasmic Reticulum - immunology</subject><subject>Endoplasmic Reticulum - metabolism</subject><subject>Environmental factors</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - immunology</subject><subject>Genes</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Infection</subject><subject>Infections</subject><subject>Inflammation</subject><subject>Integration</subject><subject>Interleukin 12</subject><subject>Interleukin 23</subject><subject>Interleukin-23 - immunology</subject><subject>Interleukin-23 - metabolism</subject><subject>Messenger RNA</subject><subject>Monocytes</subject><subject>Myeloid cells</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Pathogens</subject><subject>Pattern recognition</subject><subject>Promoters</subject><subject>Proteins</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Secretion</subject><subject>Stress</subject><subject>Stress, Physiological - immunology</subject><subject>Toll-like receptors</subject><subject>Transcription Factor CHOP - metabolism</subject><subject>Transcription factors</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFks1vFCEYh4nR2LV69qQhXvTQscDweTExm2qbbFIPeiYMA8pmBkaYafS_l8mubfWgJwg87xPelx8AzzF6i5Foz6doSt1hLFpeDx6ADUYKN5wq9BBsECKikZTQE_CklD1CSDGJHoMTgqTgGNMNSBexT9NgyhgszG4OdhmWEZY5u1KaEPvFuh7O2cRic5jmkCL0xs4pn8Ht5fWnMxgKtHmxwQzQpwx7F_scqgdaNwzwateQFrof0-qrxU_BI2-G4p4d11Pw5cPF5-1ls7v-eLV9v2ssU2JupLfUG2qV6HxLie-U8AITrpjvkTRGENp3bc-8cBxTY2WnjGGIuMoR3OP2FLw7eKelG11vXaw9DHrKYTT5p04m6D9vYvimv6YbTRRjSPEqeH0U5PR9cWXWYyhrSya6tBQt64ypVAz_lxRM4pYKJCv55p8kply2nCiySl_9he7TkmMd2erjpP7s-sbzA2RzKiU7f9sfRnrNh17zoe_yUSte3h_LLf87EBWAR2CtvNMJTbHGgqu1ixcHZF9qDO4phESsPv0XY6_LnQ</recordid><startdate>20101012</startdate><enddate>20101012</enddate><creator>Goodall, Jane C.</creator><creator>Wu, Changxin</creator><creator>Zhang, Yongsheng</creator><creator>McNeill, Louise</creator><creator>Ellis, Lou</creator><creator>Saudek, Vladimir</creator><creator>Gaston, J. 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S. Hill</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endoplasmic reticulum stress-induced transcription factor, CHOP, is crucial for dendritic cell IL-23 expression</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2010-10-12</date><risdate>2010</risdate><volume>107</volume><issue>41</issue><spage>17698</spage><epage>17703</epage><pages>17698-17703</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>The endoplasmic reticulum (ER) stress response detects malfunctions in cellular physiology, and microbial pattern recognition receptors recognize external threats posed by infectious agents. This study has investigated whether proinflammatory cytokine expression by monocyte-derived dendritic cells is affected by the induction of ER stress. Activation of ER stress, in combination with Toll-like receptor (TLR) agonists, markedly enhanced expression of mRNA of the unique p19 subunit of IL-23, and also significantly augmented secretion of IL-23 protein. These effects were not seen for IL-12 secretion. The IL-23 gene was found to be a target of the ER stress-induced transcription factor C/EBP homologous protein (CHOP), which exhibited enhanced binding in the context of both ER stress and TLR stimulation. Knockdown of CHOP in U937 cells significantly reduced the synergistic effects of TLR and ER stress on IL-23p19 expression, but did not affect expression of other LPS-responsive genes. The integration of ER stress signals and the requirement for CHOP in the induction of IL-23 responses was also investigated in a physiological setting: infection of myeloid cells with Chlamydia trachomatis resulted in the expression of CHOP mRNA and induced the binding of CHOP to the IL-23 promoter. 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| subjects | Agonists Binding sites Biological Sciences CCAAT/enhancer-binding protein Cell Line, Tumor Cells Chlamydia Infections - immunology Chlamydia trachomatis Chromatin Immunoprecipitation Cytokines Dendritic cells Dendritic Cells - immunology Endoplasmic reticulum Endoplasmic Reticulum - immunology Endoplasmic Reticulum - metabolism Environmental factors Enzyme-Linked Immunosorbent Assay Gene expression Gene Expression Regulation - immunology Genes Humans Immune response Immune system Infection Infections Inflammation Integration Interleukin 12 Interleukin 23 Interleukin-23 - immunology Interleukin-23 - metabolism Messenger RNA Monocytes Myeloid cells Oligonucleotide Array Sequence Analysis Pathogens Pattern recognition Promoters Proteins Ribonucleic acid RNA Secretion Stress Stress, Physiological - immunology Toll-like receptors Transcription Factor CHOP - metabolism Transcription factors |
| title | Endoplasmic reticulum stress-induced transcription factor, CHOP, is crucial for dendritic cell IL-23 expression |
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