Human herpesvirus 6A partially suppresses functional properties of DC without viral replication
Human herpesvirus 6A (HHV-6A) is a common virus with a worldwide distribution that has been associated with multiple sclerosis. Whether HHV-6A can replicate in dendritic cells (DC) and how the infection might modulate the functional properties of the cell are currently not well known and need furthe...
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| Veröffentlicht in: | PloS one 2013-03, Vol.8 (3), p.e58122-e58122 |
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| creator | Gustafsson, Rasmus K L Engdahl, Elin E Hammarfjord, Oscar Adikari, Sanjaya B Lourda, Magda Klingström, Jonas Svensson, Mattias Fogdell-Hahn, Anna |
| description | Human herpesvirus 6A (HHV-6A) is a common virus with a worldwide distribution that has been associated with multiple sclerosis. Whether HHV-6A can replicate in dendritic cells (DC) and how the infection might modulate the functional properties of the cell are currently not well known and need further investigations. Here, we show that a non-productive infection of HHV-6A in DC leads to the up-regulation of HLA-ABC, via autocrine IFN-α signaling, as well as the up-regulation of HLA-DR and CD86. However, HHV-6A exposure reduces IL-8 secretion by DC and their capacity to stimulate allogenic T cell proliferation. The ability to suppress DC functions important for activation of innate and adaptive immune responses might be one successful strategy by which HHV-6A avoids the induction of appropriate host defense mechanisms, and thus facilitating persistent infection. |
| doi_str_mv | 10.1371/journal.pone.0058122 |
| format | Article |
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Whether HHV-6A can replicate in dendritic cells (DC) and how the infection might modulate the functional properties of the cell are currently not well known and need further investigations. Here, we show that a non-productive infection of HHV-6A in DC leads to the up-regulation of HLA-ABC, via autocrine IFN-α signaling, as well as the up-regulation of HLA-DR and CD86. However, HHV-6A exposure reduces IL-8 secretion by DC and their capacity to stimulate allogenic T cell proliferation. The ability to suppress DC functions important for activation of innate and adaptive immune responses might be one successful strategy by which HHV-6A avoids the induction of appropriate host defense mechanisms, and thus facilitating persistent infection.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0058122</identifier><identifier>PMID: 23526966</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adaptive Immunity ; Analysis ; Autocrine signalling ; B cells ; Biology ; CD4-Positive T-Lymphocytes - immunology ; CD8-Positive T-Lymphocytes - immunology ; CD86 antigen ; Cell activation ; Cell growth ; Cell proliferation ; Cytokines ; Cytokines - biosynthesis ; Dendritic cells ; Dendritic Cells - immunology ; Dendritic Cells - virology ; Gene expression ; Health aspects ; Herpesvirus 6, Human - immunology ; Herpesvirus 6, Human - pathogenicity ; Herpesvirus 6, Human - physiology ; Histocompatibility antigen HLA ; HLA Antigens - metabolism ; Host-Pathogen Interactions - immunology ; Humans ; Immune response ; Immune Tolerance ; Immunity, Innate ; Infection ; Infections ; Inflammation Mediators - metabolism ; Interferon ; Interferon-alpha - metabolism ; Interleukin 8 ; Interleukin-4 - biosynthesis ; Lymphocytes ; Lymphocytes T ; Medical research ; Medicine ; Multiple sclerosis ; Nervous system ; Neurosciences ; R&D ; Research & development ; T cell receptors ; T cells ; Tumor necrosis factor-TNF ; Virus Replication ; Viruses</subject><ispartof>PloS one, 2013-03, Vol.8 (3), p.e58122-e58122</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Gustafsson et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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The ability to suppress DC functions important for activation of innate and adaptive immune responses might be one successful strategy by which HHV-6A avoids the induction of appropriate host defense mechanisms, and thus facilitating persistent infection.</description><subject>Adaptive Immunity</subject><subject>Analysis</subject><subject>Autocrine signalling</subject><subject>B cells</subject><subject>Biology</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>CD8-Positive T-Lymphocytes - immunology</subject><subject>CD86 antigen</subject><subject>Cell activation</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Cytokines</subject><subject>Cytokines - biosynthesis</subject><subject>Dendritic cells</subject><subject>Dendritic Cells - immunology</subject><subject>Dendritic Cells - virology</subject><subject>Gene expression</subject><subject>Health aspects</subject><subject>Herpesvirus 6, Human - immunology</subject><subject>Herpesvirus 6, Human - 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Whether HHV-6A can replicate in dendritic cells (DC) and how the infection might modulate the functional properties of the cell are currently not well known and need further investigations. Here, we show that a non-productive infection of HHV-6A in DC leads to the up-regulation of HLA-ABC, via autocrine IFN-α signaling, as well as the up-regulation of HLA-DR and CD86. However, HHV-6A exposure reduces IL-8 secretion by DC and their capacity to stimulate allogenic T cell proliferation. The ability to suppress DC functions important for activation of innate and adaptive immune responses might be one successful strategy by which HHV-6A avoids the induction of appropriate host defense mechanisms, and thus facilitating persistent infection.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23526966</pmid><doi>10.1371/journal.pone.0058122</doi><tpages>e58122</tpages><oa>free_for_read</oa></addata></record> |
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| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; SWEPUB Freely available online; Free Full-Text Journals in Chemistry |
| subjects | Adaptive Immunity Analysis Autocrine signalling B cells Biology CD4-Positive T-Lymphocytes - immunology CD8-Positive T-Lymphocytes - immunology CD86 antigen Cell activation Cell growth Cell proliferation Cytokines Cytokines - biosynthesis Dendritic cells Dendritic Cells - immunology Dendritic Cells - virology Gene expression Health aspects Herpesvirus 6, Human - immunology Herpesvirus 6, Human - pathogenicity Herpesvirus 6, Human - physiology Histocompatibility antigen HLA HLA Antigens - metabolism Host-Pathogen Interactions - immunology Humans Immune response Immune Tolerance Immunity, Innate Infection Infections Inflammation Mediators - metabolism Interferon Interferon-alpha - metabolism Interleukin 8 Interleukin-4 - biosynthesis Lymphocytes Lymphocytes T Medical research Medicine Multiple sclerosis Nervous system Neurosciences R&D Research & development T cell receptors T cells Tumor necrosis factor-TNF Virus Replication Viruses |
| title | Human herpesvirus 6A partially suppresses functional properties of DC without viral replication |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-27T11%3A03%3A29IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Human%20herpesvirus%206A%20partially%20suppresses%20functional%20properties%20of%20DC%20without%20viral%20replication&rft.jtitle=PloS%20one&rft.au=Gustafsson,%20Rasmus%20K%20L&rft.date=2013-03-05&rft.volume=8&rft.issue=3&rft.spage=e58122&rft.epage=e58122&rft.pages=e58122-e58122&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0058122&rft_dat=%3Cgale_plos_%3EA478416349%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1330880567&rft_id=info:pmid/23526966&rft_galeid=A478416349&rft_doaj_id=oai_doaj_org_article_7886d2dbf57d4d33b06f783c64db3b48&rfr_iscdi=true |