Semaphorin 7A Promotes Chemokine-Driven Dendritic Cell Migration
Dendritic cell (DC) migration is essential for efficient host defense against pathogens and cancer, as well as for the efficacy of DC-based immunotherapies. However, the molecules that induce the migratory phenotype of DCs are poorly defined. Based on a large-scale proteome analysis of maturing DCs,...
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Veröffentlicht in: | The Journal of immunology (1950) 2016-01, Vol.196 (1), p.459-468 |
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creator | van Rijn, Anoek Paulis, Leonie te Riet, Joost Vasaturo, Angela Reinieren-Beeren, Inge van der Schaaf, Alie Kuipers, Arthur J Schulte, Luuk P Jongbloets, Bart C Pasterkamp, R Jeroen Figdor, Carl G van Spriel, Annemiek B Buschow, Sonja I |
description | Dendritic cell (DC) migration is essential for efficient host defense against pathogens and cancer, as well as for the efficacy of DC-based immunotherapies. However, the molecules that induce the migratory phenotype of DCs are poorly defined. Based on a large-scale proteome analysis of maturing DCs, we identified the GPI-anchored protein semaphorin 7A (Sema7A) as being highly expressed on activated primary myeloid and plasmacytoid DCs in human and mouse. We demonstrate that Sema7A deficiency results in impaired chemokine CCL21-driven DC migration in vivo. Impaired formation of actin-based protrusions, resulting in slower three-dimensional migration, was identified as the mechanism underlying the DC migration defect. Furthermore, we show, by atomic force microscopy, that Sema7A decreases adhesion strength to extracellular matrix while increasing the connectivity of adhesion receptors to the actin cytoskeleton. This study demonstrates that Sema7A controls the assembly of actin-based protrusions that drive DC migration in response to CCL21. |
doi_str_mv | 10.4049/jimmunol.1403096 |
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However, the molecules that induce the migratory phenotype of DCs are poorly defined. Based on a large-scale proteome analysis of maturing DCs, we identified the GPI-anchored protein semaphorin 7A (Sema7A) as being highly expressed on activated primary myeloid and plasmacytoid DCs in human and mouse. We demonstrate that Sema7A deficiency results in impaired chemokine CCL21-driven DC migration in vivo. Impaired formation of actin-based protrusions, resulting in slower three-dimensional migration, was identified as the mechanism underlying the DC migration defect. Furthermore, we show, by atomic force microscopy, that Sema7A decreases adhesion strength to extracellular matrix while increasing the connectivity of adhesion receptors to the actin cytoskeleton. This study demonstrates that Sema7A controls the assembly of actin-based protrusions that drive DC migration in response to CCL21.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.1403096</identifier><identifier>PMID: 26597008</identifier><language>eng</language><publisher>United States</publisher><subject>Actin Cytoskeleton - metabolism ; Animals ; Antigens, CD - genetics ; Antigens, CD - physiology ; Cell Adhesion ; Cell Movement - genetics ; Cell Movement - physiology ; Cells, Cultured ; Chemokine CCL21 - metabolism ; Dendritic Cells - physiology ; Extracellular Matrix - metabolism ; GPI-Linked Proteins - genetics ; GPI-Linked Proteins - physiology ; Humans ; Mice ; Mice, Knockout ; Microscopy, Atomic Force ; RNA Interference ; RNA, Small Interfering ; Semaphorins - genetics ; Semaphorins - physiology</subject><ispartof>The Journal of immunology (1950), 2016-01, Vol.196 (1), p.459-468</ispartof><rights>Copyright © 2015 by The American Association of Immunologists, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c374t-12c32b25b968a0be134a81e39fd3bbc07012b711e0b9123e77050f68624a4d9c3</citedby><cites>FETCH-LOGICAL-c374t-12c32b25b968a0be134a81e39fd3bbc07012b711e0b9123e77050f68624a4d9c3</cites><orcidid>0000-0003-2678-6024 ; 0000-0002-9093-010X ; 0000-0003-4799-333X ; 0000-0003-1631-6440 ; 0000-0001-8030-1572</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26597008$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>van Rijn, Anoek</creatorcontrib><creatorcontrib>Paulis, Leonie</creatorcontrib><creatorcontrib>te Riet, Joost</creatorcontrib><creatorcontrib>Vasaturo, Angela</creatorcontrib><creatorcontrib>Reinieren-Beeren, Inge</creatorcontrib><creatorcontrib>van der Schaaf, Alie</creatorcontrib><creatorcontrib>Kuipers, Arthur J</creatorcontrib><creatorcontrib>Schulte, Luuk P</creatorcontrib><creatorcontrib>Jongbloets, Bart C</creatorcontrib><creatorcontrib>Pasterkamp, R Jeroen</creatorcontrib><creatorcontrib>Figdor, Carl G</creatorcontrib><creatorcontrib>van Spriel, Annemiek B</creatorcontrib><creatorcontrib>Buschow, Sonja I</creatorcontrib><title>Semaphorin 7A Promotes Chemokine-Driven Dendritic Cell Migration</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>Dendritic cell (DC) migration is essential for efficient host defense against pathogens and cancer, as well as for the efficacy of DC-based immunotherapies. 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Paulis, Leonie ; te Riet, Joost ; Vasaturo, Angela ; Reinieren-Beeren, Inge ; van der Schaaf, Alie ; Kuipers, Arthur J ; Schulte, Luuk P ; Jongbloets, Bart C ; Pasterkamp, R Jeroen ; Figdor, Carl G ; van Spriel, Annemiek B ; Buschow, Sonja I</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c374t-12c32b25b968a0be134a81e39fd3bbc07012b711e0b9123e77050f68624a4d9c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Actin Cytoskeleton - metabolism</topic><topic>Animals</topic><topic>Antigens, CD - genetics</topic><topic>Antigens, CD - physiology</topic><topic>Cell Adhesion</topic><topic>Cell Movement - genetics</topic><topic>Cell Movement - physiology</topic><topic>Cells, Cultured</topic><topic>Chemokine CCL21 - metabolism</topic><topic>Dendritic Cells - physiology</topic><topic>Extracellular Matrix - metabolism</topic><topic>GPI-Linked Proteins - genetics</topic><topic>GPI-Linked Proteins - physiology</topic><topic>Humans</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Microscopy, Atomic Force</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering</topic><topic>Semaphorins - genetics</topic><topic>Semaphorins - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>van Rijn, Anoek</creatorcontrib><creatorcontrib>Paulis, Leonie</creatorcontrib><creatorcontrib>te Riet, Joost</creatorcontrib><creatorcontrib>Vasaturo, Angela</creatorcontrib><creatorcontrib>Reinieren-Beeren, Inge</creatorcontrib><creatorcontrib>van der Schaaf, Alie</creatorcontrib><creatorcontrib>Kuipers, Arthur J</creatorcontrib><creatorcontrib>Schulte, Luuk P</creatorcontrib><creatorcontrib>Jongbloets, Bart C</creatorcontrib><creatorcontrib>Pasterkamp, R Jeroen</creatorcontrib><creatorcontrib>Figdor, Carl G</creatorcontrib><creatorcontrib>van Spriel, Annemiek B</creatorcontrib><creatorcontrib>Buschow, Sonja I</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>van Rijn, Anoek</au><au>Paulis, Leonie</au><au>te Riet, Joost</au><au>Vasaturo, Angela</au><au>Reinieren-Beeren, Inge</au><au>van der Schaaf, Alie</au><au>Kuipers, Arthur J</au><au>Schulte, Luuk P</au><au>Jongbloets, Bart C</au><au>Pasterkamp, R Jeroen</au><au>Figdor, Carl G</au><au>van Spriel, Annemiek B</au><au>Buschow, Sonja I</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Semaphorin 7A Promotes Chemokine-Driven Dendritic Cell Migration</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>2016-01-01</date><risdate>2016</risdate><volume>196</volume><issue>1</issue><spage>459</spage><epage>468</epage><pages>459-468</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><abstract>Dendritic cell (DC) migration is essential for efficient host defense against pathogens and cancer, as well as for the efficacy of DC-based immunotherapies. 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subjects | Actin Cytoskeleton - metabolism Animals Antigens, CD - genetics Antigens, CD - physiology Cell Adhesion Cell Movement - genetics Cell Movement - physiology Cells, Cultured Chemokine CCL21 - metabolism Dendritic Cells - physiology Extracellular Matrix - metabolism GPI-Linked Proteins - genetics GPI-Linked Proteins - physiology Humans Mice Mice, Knockout Microscopy, Atomic Force RNA Interference RNA, Small Interfering Semaphorins - genetics Semaphorins - physiology |
title | Semaphorin 7A Promotes Chemokine-Driven Dendritic Cell Migration |
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