Continuous Expression of the Transcription Factor E2-2 Maintains the Cell Fate of Mature Plasmacytoid Dendritic Cells
The interferon-producing plasmacytoid dendritic cells (pDCs) share common progenitors with antigen-presenting classical dendritic cells (cDCs), yet they possess distinct morphology and molecular features resembling those of lymphocytes. It is unclear whether the unique cell fate of pDCs is actively...
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| Veröffentlicht in: | Immunity (Cambridge, Mass.) Mass.), 2010-12, Vol.33 (6), p.905-916 |
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| creator | Ghosh, Hiyaa S. Cisse, Babacar Bunin, Anna Lewis, Kanako L. Reizis, Boris |
| description | The interferon-producing plasmacytoid dendritic cells (pDCs) share common progenitors with antigen-presenting classical dendritic cells (cDCs), yet they possess distinct morphology and molecular features resembling those of lymphocytes. It is unclear whether the unique cell fate of pDCs is actively maintained in the steady state. We report that the deletion of transcription factor E2-2 from mature peripheral pDCs caused their spontaneous differentiation into cells with cDC properties. This included the loss of pDC markers, increase in MHC class II expression and T cell priming capacity, acquisition of dendritic morphology, and induction of cDC signature genes. Genome-wide chromatin immunoprecipitation revealed direct binding of E2-2 to key pDC-specific and lymphoid genes, as well as to certain genes enriched in cDCs. Thus, E2-2 actively maintains the cell fate of mature pDCs and opposes the “default” cDC fate, in part through direct regulation of lineage-specific gene expression programs.
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► Deletion of E2-2 from mature pDCs causes phenotypic conversion to cDC-like cells ► E2-2-deficient pDCs acquire the morphology and gene expression signature of cDCs ► E2-2 directly binds to multiple pDC-enriched target genes ► E2-2 maintains Bcl11a and represses Id2 expression in pDCs |
| doi_str_mv | 10.1016/j.immuni.2010.11.023 |
| format | Article |
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[Display omitted]
► Deletion of E2-2 from mature pDCs causes phenotypic conversion to cDC-like cells ► E2-2-deficient pDCs acquire the morphology and gene expression signature of cDCs ► E2-2 directly binds to multiple pDC-enriched target genes ► E2-2 maintains Bcl11a and represses Id2 expression in pDCs</description><identifier>ISSN: 1074-7613</identifier><identifier>ISSN: 1097-4180</identifier><identifier>EISSN: 1097-4180</identifier><identifier>DOI: 10.1016/j.immuni.2010.11.023</identifier><identifier>PMID: 21145760</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Antigen Presentation - genetics ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - genetics ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - immunology ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - metabolism ; Cell Differentiation - genetics ; Cell Differentiation - immunology ; Cell Lineage - genetics ; Cell Lineage - immunology ; Cell Separation ; Cell Transdifferentiation - genetics ; Cell Transdifferentiation - immunology ; Cells, Cultured ; Dendritic Cells - immunology ; Dendritic Cells - metabolism ; Dendritic Cells - pathology ; Flow Cytometry ; Gene expression ; Gene Expression Profiling ; Gene Expression Regulation, Developmental - genetics ; Gene Expression Regulation, Developmental - immunology ; Immune system ; Ligands ; Lymphocytes ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Proteins ; Rodents ; Transcription Factor 4 ; Transcription factors</subject><ispartof>Immunity (Cambridge, Mass.), 2010-12, Vol.33 (6), p.905-916</ispartof><rights>2010 Elsevier Inc.</rights><rights>Copyright Elsevier Limited Dec 14, 2010</rights><rights>2010 Elsevier Inc. All rights reserved. 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c588t-693a03f8672d1bd9664091f3cf13e9db7561336e54edfd7f0ebfccb188ed20f63</citedby><cites>FETCH-LOGICAL-c588t-693a03f8672d1bd9664091f3cf13e9db7561336e54edfd7f0ebfccb188ed20f63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S107476131000453X$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21145760$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ghosh, Hiyaa S.</creatorcontrib><creatorcontrib>Cisse, Babacar</creatorcontrib><creatorcontrib>Bunin, Anna</creatorcontrib><creatorcontrib>Lewis, Kanako L.</creatorcontrib><creatorcontrib>Reizis, Boris</creatorcontrib><title>Continuous Expression of the Transcription Factor E2-2 Maintains the Cell Fate of Mature Plasmacytoid Dendritic Cells</title><title>Immunity (Cambridge, Mass.)</title><addtitle>Immunity</addtitle><description>The interferon-producing plasmacytoid dendritic cells (pDCs) share common progenitors with antigen-presenting classical dendritic cells (cDCs), yet they possess distinct morphology and molecular features resembling those of lymphocytes. It is unclear whether the unique cell fate of pDCs is actively maintained in the steady state. We report that the deletion of transcription factor E2-2 from mature peripheral pDCs caused their spontaneous differentiation into cells with cDC properties. This included the loss of pDC markers, increase in MHC class II expression and T cell priming capacity, acquisition of dendritic morphology, and induction of cDC signature genes. Genome-wide chromatin immunoprecipitation revealed direct binding of E2-2 to key pDC-specific and lymphoid genes, as well as to certain genes enriched in cDCs. Thus, E2-2 actively maintains the cell fate of mature pDCs and opposes the “default” cDC fate, in part through direct regulation of lineage-specific gene expression programs.
[Display omitted]
► Deletion of E2-2 from mature pDCs causes phenotypic conversion to cDC-like cells ► E2-2-deficient pDCs acquire the morphology and gene expression signature of cDCs ► E2-2 directly binds to multiple pDC-enriched target genes ► E2-2 maintains Bcl11a and represses Id2 expression in pDCs</description><subject>Animals</subject><subject>Antigen Presentation - genetics</subject><subject>Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - genetics</subject><subject>Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - immunology</subject><subject>Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - metabolism</subject><subject>Cell Differentiation - genetics</subject><subject>Cell Differentiation - immunology</subject><subject>Cell Lineage - genetics</subject><subject>Cell Lineage - immunology</subject><subject>Cell Separation</subject><subject>Cell Transdifferentiation - genetics</subject><subject>Cell Transdifferentiation - immunology</subject><subject>Cells, Cultured</subject><subject>Dendritic Cells - immunology</subject><subject>Dendritic Cells - metabolism</subject><subject>Dendritic Cells - pathology</subject><subject>Flow Cytometry</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Developmental - genetics</subject><subject>Gene Expression Regulation, Developmental - immunology</subject><subject>Immune system</subject><subject>Ligands</subject><subject>Lymphocytes</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Transcription Factor 4</subject><subject>Transcription factors</subject><issn>1074-7613</issn><issn>1097-4180</issn><issn>1097-4180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkk1v1DAQhiMEoh_wDxCKxIFTlrGd2MkFCS3bgtQKDuVsOfaYerWxF9up6L_H6ZbycYCDZWvmmbHn9VtVLwisCBD-Zrty0zR7t6KwhMgKKHtUHRMYRNOSHh4vZ9E2ghN2VJ2ktAUgbTfA0-qIknISHI6reR18dn4Oc6o33_cRU3LB18HW-Rrrq6h80tHt8xI8UzqHWG9oQ-tL5XwuK91xa9ztSjrjUnip8hyx_rxTaVL6Ngdn6vfoTXTZ6Ts0PaueWLVL-Px-P62-nG2u1h-ai0_nH9fvLhrd9X1u-MAUMNtzQQ0ZzcB5CwOxTFvCcDCj6MpsjGPXorFGWMDRaj2SvkdDwXJ2Wr099N3P44RGo89R7eQ-uknFWxmUk39mvLuWX8ONZEVTKkRp8Pq-QQzfZkxZTi7pMoLyWCSTQxGaD337f7KnIAbooC3kq7_IbZijLzpI0nVAKGU9LVR7oHQMKUW0D68mIBcDyK08GEAuBpCEyGKAUvby94kfin7--C9JsOh-4zDKpB16jcZF1Fma4P59ww_OdMS5</recordid><startdate>20101214</startdate><enddate>20101214</enddate><creator>Ghosh, Hiyaa S.</creator><creator>Cisse, Babacar</creator><creator>Bunin, Anna</creator><creator>Lewis, Kanako L.</creator><creator>Reizis, Boris</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20101214</creationdate><title>Continuous Expression of the Transcription Factor E2-2 Maintains the Cell Fate of Mature Plasmacytoid Dendritic Cells</title><author>Ghosh, Hiyaa S. ; 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It is unclear whether the unique cell fate of pDCs is actively maintained in the steady state. We report that the deletion of transcription factor E2-2 from mature peripheral pDCs caused their spontaneous differentiation into cells with cDC properties. This included the loss of pDC markers, increase in MHC class II expression and T cell priming capacity, acquisition of dendritic morphology, and induction of cDC signature genes. Genome-wide chromatin immunoprecipitation revealed direct binding of E2-2 to key pDC-specific and lymphoid genes, as well as to certain genes enriched in cDCs. Thus, E2-2 actively maintains the cell fate of mature pDCs and opposes the “default” cDC fate, in part through direct regulation of lineage-specific gene expression programs.
[Display omitted]
► Deletion of E2-2 from mature pDCs causes phenotypic conversion to cDC-like cells ► E2-2-deficient pDCs acquire the morphology and gene expression signature of cDCs ► E2-2 directly binds to multiple pDC-enriched target genes ► E2-2 maintains Bcl11a and represses Id2 expression in pDCs</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>21145760</pmid><doi>10.1016/j.immuni.2010.11.023</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antigen Presentation - genetics Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - genetics Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - immunology Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - metabolism Cell Differentiation - genetics Cell Differentiation - immunology Cell Lineage - genetics Cell Lineage - immunology Cell Separation Cell Transdifferentiation - genetics Cell Transdifferentiation - immunology Cells, Cultured Dendritic Cells - immunology Dendritic Cells - metabolism Dendritic Cells - pathology Flow Cytometry Gene expression Gene Expression Profiling Gene Expression Regulation, Developmental - genetics Gene Expression Regulation, Developmental - immunology Immune system Ligands Lymphocytes Mice Mice, Inbred C57BL Mice, Knockout Proteins Rodents Transcription Factor 4 Transcription factors |
| title | Continuous Expression of the Transcription Factor E2-2 Maintains the Cell Fate of Mature Plasmacytoid Dendritic Cells |
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