Klebsiella pneumoniae‐triggered DC recruit human NK cells in a CCR5‐dependent manner leading to increased CCL19‐responsiveness and activation of NK cells
Besides their role in destruction of altered self‐cells, NK cells have been shown to potentiate T‐cell responses by interacting with DC. To take advantage of NK-DC crosstalk in therapeutic DC‐based vaccination for infectious diseases and cancer, it is essential to understand the biology of this cros...
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Veröffentlicht in: | European journal of immunology 2010-11, Vol.40 (11), p.3138-3149 |
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creator | Van Elssen, Catharina H.M.J Vanderlocht, Joris Frings, Peter W.H Senden‐Gijsbers, Birgit L.M.G Schnijderberg, Melanie C.A van Gelder, Michel Meek, Bob Libon, Christine Ferlazzo, Guido Germeraad, Wilfred T.V Bos, Gerard M.J |
description | Besides their role in destruction of altered self‐cells, NK cells have been shown to potentiate T‐cell responses by interacting with DC. To take advantage of NK-DC crosstalk in therapeutic DC‐based vaccination for infectious diseases and cancer, it is essential to understand the biology of this crosstalk. We aimed to elucidate the in vitro mechanisms responsible for NK‐cell recruitment and activation by DC during infection. To mimic bacterial infection, DC were exposed to a membrane fraction of Klebsiella pneumoniae, which triggers TLR2/4. DC matured with these bacterial fragments can actively recruit NK cells in a CCR5‐dependent manner. An additional mechanism of DC‐induced NK‐cell recruitment is characterized by the induction of CCR7 expression on CD56dimCD16⁺ NK cells after physical contact with membrane fraction of K. pneumoniae‐matured DC, resulting in an enhanced migratory responsiveness to the lymph node‐associated chemokine CCL19. Bacterial fragment‐matured DC do not only mediate NK‐cell migration but also meet the prerequisites needed for augmentation of NK‐cell cytotoxicity and IFN‐γ production, the latter of which contributes to Th1 polarization. |
doi_str_mv | 10.1002/eji.201040496 |
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To take advantage of NK-DC crosstalk in therapeutic DC‐based vaccination for infectious diseases and cancer, it is essential to understand the biology of this crosstalk. We aimed to elucidate the in vitro mechanisms responsible for NK‐cell recruitment and activation by DC during infection. To mimic bacterial infection, DC were exposed to a membrane fraction of Klebsiella pneumoniae, which triggers TLR2/4. DC matured with these bacterial fragments can actively recruit NK cells in a CCR5‐dependent manner. An additional mechanism of DC‐induced NK‐cell recruitment is characterized by the induction of CCR7 expression on CD56dimCD16⁺ NK cells after physical contact with membrane fraction of K. pneumoniae‐matured DC, resulting in an enhanced migratory responsiveness to the lymph node‐associated chemokine CCL19. Bacterial fragment‐matured DC do not only mediate NK‐cell migration but also meet the prerequisites needed for augmentation of NK‐cell cytotoxicity and IFN‐γ production, the latter of which contributes to Th1 polarization.</description><identifier>ISSN: 0014-2980</identifier><identifier>EISSN: 1521-4141</identifier><identifier>DOI: 10.1002/eji.201040496</identifier><identifier>PMID: 20865789</identifier><identifier>CODEN: EJIMAF</identifier><language>eng</language><publisher>Weinheim: Wiley‐VCH Verlag</publisher><subject>Bacterial infections ; CCR5 ; CCR7 ; Cell Movement - immunology ; Cells, Cultured ; Chemokine CCL19 - immunology ; Dendritic Cells - immunology ; Gene Expression Regulation - immunology ; Humans ; Interferon-gamma - immunology ; Killer Cells, Natural - immunology ; Klebsiella Infections - immunology ; Klebsiella pneumoniae ; Klebsiella pneumoniae - immunology ; Lymphocyte Activation - immunology ; NK–DC interaction ; Receptors, CCR5 - immunology ; Receptors, CCR7 - immunology ; Th1 Cells - immunology ; Th1 polarization ; Toll-Like Receptor 2 - immunology ; Toll-Like Receptor 4 - immunology</subject><ispartof>European journal of immunology, 2010-11, Vol.40 (11), p.3138-3149</ispartof><rights>Copyright © 2010 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim</rights><rights>Copyright © 2010 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.</rights><rights>Copyright © 2010 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5306-4088e1be50849c86fb26e05367bcc1b7cc0ce753ccc9c589b3f2e8adc8f511453</citedby><cites>FETCH-LOGICAL-c5306-4088e1be50849c86fb26e05367bcc1b7cc0ce753ccc9c589b3f2e8adc8f511453</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Feji.201040496$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Feji.201040496$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20865789$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Van Elssen, Catharina H.M.J</creatorcontrib><creatorcontrib>Vanderlocht, Joris</creatorcontrib><creatorcontrib>Frings, Peter W.H</creatorcontrib><creatorcontrib>Senden‐Gijsbers, Birgit L.M.G</creatorcontrib><creatorcontrib>Schnijderberg, Melanie C.A</creatorcontrib><creatorcontrib>van Gelder, Michel</creatorcontrib><creatorcontrib>Meek, Bob</creatorcontrib><creatorcontrib>Libon, Christine</creatorcontrib><creatorcontrib>Ferlazzo, Guido</creatorcontrib><creatorcontrib>Germeraad, Wilfred T.V</creatorcontrib><creatorcontrib>Bos, Gerard M.J</creatorcontrib><title>Klebsiella pneumoniae‐triggered DC recruit human NK cells in a CCR5‐dependent manner leading to increased CCL19‐responsiveness and activation of NK cells</title><title>European journal of immunology</title><addtitle>Eur J Immunol</addtitle><description>Besides their role in destruction of altered self‐cells, NK cells have been shown to potentiate T‐cell responses by interacting with DC. To take advantage of NK-DC crosstalk in therapeutic DC‐based vaccination for infectious diseases and cancer, it is essential to understand the biology of this crosstalk. We aimed to elucidate the in vitro mechanisms responsible for NK‐cell recruitment and activation by DC during infection. To mimic bacterial infection, DC were exposed to a membrane fraction of Klebsiella pneumoniae, which triggers TLR2/4. DC matured with these bacterial fragments can actively recruit NK cells in a CCR5‐dependent manner. An additional mechanism of DC‐induced NK‐cell recruitment is characterized by the induction of CCR7 expression on CD56dimCD16⁺ NK cells after physical contact with membrane fraction of K. pneumoniae‐matured DC, resulting in an enhanced migratory responsiveness to the lymph node‐associated chemokine CCL19. Bacterial fragment‐matured DC do not only mediate NK‐cell migration but also meet the prerequisites needed for augmentation of NK‐cell cytotoxicity and IFN‐γ production, the latter of which contributes to Th1 polarization.</description><subject>Bacterial infections</subject><subject>CCR5</subject><subject>CCR7</subject><subject>Cell Movement - immunology</subject><subject>Cells, Cultured</subject><subject>Chemokine CCL19 - immunology</subject><subject>Dendritic Cells - immunology</subject><subject>Gene Expression Regulation - immunology</subject><subject>Humans</subject><subject>Interferon-gamma - immunology</subject><subject>Killer Cells, Natural - immunology</subject><subject>Klebsiella Infections - immunology</subject><subject>Klebsiella pneumoniae</subject><subject>Klebsiella pneumoniae - immunology</subject><subject>Lymphocyte Activation - immunology</subject><subject>NK–DC interaction</subject><subject>Receptors, CCR5 - immunology</subject><subject>Receptors, CCR7 - immunology</subject><subject>Th1 Cells - immunology</subject><subject>Th1 polarization</subject><subject>Toll-Like Receptor 2 - immunology</subject><subject>Toll-Like Receptor 4 - immunology</subject><issn>0014-2980</issn><issn>1521-4141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90ctu1DAUBmALgehQWLIFSyxgk3Kc-LpEoUDpCCSg68hxTgaPMk6wk6LueATegHfjSXA1ZYRYdOWFv_P78hPymMEJAyhf4taflMCAAzfyDlkxUbKCM87ukhUA40VpNByRByltAcBIYe6ToxK0FEqbFfl1PmCbPA6DpVPAZTcGb_H3j59z9JsNRuzo65pGdHHxM_267GygH86pywOJ-kAtretPIvsOJwwdhplmEjDSAW3nw4bOY3Yuok05q67XzGQdMU1jSP4SA6ZEbeiodbO_tLMfAx37wxkPyb3eDgkf3azH5OLN6Zf6XbH--PasfrUunKhAFhy0RtaiAM2N07JvS4kgKqla51irnAOHSlTOOeOENm3Vl6ht53QvGOOiOibP97lTHL8tmOZm59P1DWzAcUmNklWZf0ypLF_cKplSUnKpJc_02X90Oy4x5HdkJaVmotIyq2KvXBxTitg3U_Q7G68aBs11x03uuDl0nP2Tm9Sl3WF30H9LzUDtwXc_4NXtac3p-7N_o5_uJ3s7NnYTfWouPuftCphhlVFQ_QFljb6M</recordid><startdate>201011</startdate><enddate>201011</enddate><creator>Van Elssen, Catharina H.M.J</creator><creator>Vanderlocht, Joris</creator><creator>Frings, Peter W.H</creator><creator>Senden‐Gijsbers, Birgit L.M.G</creator><creator>Schnijderberg, Melanie C.A</creator><creator>van Gelder, Michel</creator><creator>Meek, Bob</creator><creator>Libon, Christine</creator><creator>Ferlazzo, Guido</creator><creator>Germeraad, Wilfred T.V</creator><creator>Bos, Gerard M.J</creator><general>Wiley‐VCH Verlag</general><general>WILEY‐VCH Verlag</general><general>Wiley Subscription Services, Inc</general><scope>FBQ</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>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7QL</scope><scope>C1K</scope><scope>7X8</scope></search><sort><creationdate>201011</creationdate><title>Klebsiella pneumoniae‐triggered DC recruit human NK cells in a CCR5‐dependent manner leading to increased CCL19‐responsiveness and activation of NK cells</title><author>Van Elssen, Catharina H.M.J ; 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To take advantage of NK-DC crosstalk in therapeutic DC‐based vaccination for infectious diseases and cancer, it is essential to understand the biology of this crosstalk. We aimed to elucidate the in vitro mechanisms responsible for NK‐cell recruitment and activation by DC during infection. To mimic bacterial infection, DC were exposed to a membrane fraction of Klebsiella pneumoniae, which triggers TLR2/4. DC matured with these bacterial fragments can actively recruit NK cells in a CCR5‐dependent manner. An additional mechanism of DC‐induced NK‐cell recruitment is characterized by the induction of CCR7 expression on CD56dimCD16⁺ NK cells after physical contact with membrane fraction of K. pneumoniae‐matured DC, resulting in an enhanced migratory responsiveness to the lymph node‐associated chemokine CCL19. Bacterial fragment‐matured DC do not only mediate NK‐cell migration but also meet the prerequisites needed for augmentation of NK‐cell cytotoxicity and IFN‐γ production, the latter of which contributes to Th1 polarization.</abstract><cop>Weinheim</cop><pub>Wiley‐VCH Verlag</pub><pmid>20865789</pmid><doi>10.1002/eji.201040496</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Bacterial infections CCR5 CCR7 Cell Movement - immunology Cells, Cultured Chemokine CCL19 - immunology Dendritic Cells - immunology Gene Expression Regulation - immunology Humans Interferon-gamma - immunology Killer Cells, Natural - immunology Klebsiella Infections - immunology Klebsiella pneumoniae Klebsiella pneumoniae - immunology Lymphocyte Activation - immunology NK–DC interaction Receptors, CCR5 - immunology Receptors, CCR7 - immunology Th1 Cells - immunology Th1 polarization Toll-Like Receptor 2 - immunology Toll-Like Receptor 4 - immunology |
title | Klebsiella pneumoniae‐triggered DC recruit human NK cells in a CCR5‐dependent manner leading to increased CCL19‐responsiveness and activation of NK cells |
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