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Liver is able to activate naïve CD8+ T cells with dysfunctional anti-viral activity in the murine system
The liver possesses distinct tolerogenic properties because of continuous exposure to bacterial constituents and nonpathogenic food antigen. The central immune mediators required for the generation of effective immune responses in the liver environment have not been fully elucidated. In this report,...
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Published in: | PloS one 2009-10, Vol.4 (10), p.e7619-e7619 |
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description | The liver possesses distinct tolerogenic properties because of continuous exposure to bacterial constituents and nonpathogenic food antigen. The central immune mediators required for the generation of effective immune responses in the liver environment have not been fully elucidated. In this report, we demonstrate that the liver can indeed support effector CD8(+) T cells during adenovirus infection when the T cells are primed in secondary lymphoid tissues. In contrast, when viral antigen is delivered predominantly to the liver via intravenous (IV) adenovirus infection, intrahepatic CD8(+) T cells are significantly impaired in their ability to produce inflammatory cytokines and lyse target cells. Additionally, intrahepatic CD8(+) T cells generated during IV adenovirus infection express elevated levels of PD-1. Notably, lower doses of adenovirus infection do not rescue the impaired effector function of intrahepatic CD8(+) T cell responses. Instead, intrahepatic antigen recognition limits the generation of potent anti-viral responses at both priming and effector stages of the CD8(+) T cell response and accounts for the dysfunctional CD8(+) T cell response observed during IV adenovirus infection. These results also implicate that manipulation of antigen delivery will facilitate the design of improved vaccination strategies to persistent viral infection. |
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The central immune mediators required for the generation of effective immune responses in the liver environment have not been fully elucidated. In this report, we demonstrate that the liver can indeed support effector CD8(+) T cells during adenovirus infection when the T cells are primed in secondary lymphoid tissues. In contrast, when viral antigen is delivered predominantly to the liver via intravenous (IV) adenovirus infection, intrahepatic CD8(+) T cells are significantly impaired in their ability to produce inflammatory cytokines and lyse target cells. Additionally, intrahepatic CD8(+) T cells generated during IV adenovirus infection express elevated levels of PD-1. Notably, lower doses of adenovirus infection do not rescue the impaired effector function of intrahepatic CD8(+) T cell responses. Instead, intrahepatic antigen recognition limits the generation of potent anti-viral responses at both priming and effector stages of the CD8(+) T cell response and accounts for the dysfunctional CD8(+) T cell response observed during IV adenovirus infection. These results also implicate that manipulation of antigen delivery will facilitate the design of improved vaccination strategies to persistent viral infection.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0007619</identifier><identifier>PMID: 19876399</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adenoviridae - metabolism ; Adenoviridae Infections ; Animals ; Antiviral agents ; Antiviral Agents - chemistry ; Bacteria ; Bone Marrow Cells - cytology ; CD8 antigen ; CD8-Positive T-Lymphocytes - immunology ; CD8-Positive T-Lymphocytes - metabolism ; Cell Differentiation ; Coculture Techniques ; Cytokines ; Cytokines - metabolism ; Effector cells ; Flow Cytometry - methods ; Immune response ; Immunology/Immune Response ; Immunology/Immunity to Infections ; Immunology/Immunomodulation ; Infections ; Inflammation ; Intravenous administration ; Liver ; Liver - metabolism ; Lymphocytes ; Lymphocytes T ; Lymphoid tissue ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; PD-1 protein ; Priming ; Rodents ; Spleen - virology ; T cell receptors ; Tissues ; Vaccination ; Viral infections</subject><ispartof>PloS one, 2009-10, Vol.4 (10), p.e7619-e7619</ispartof><rights>2009 Lukens et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Lukens et al. 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c525t-6df1a4e1ab5b92d275978793f3378b1d750e0a3e05c5a24e68a64a05039c65043</citedby><cites>FETCH-LOGICAL-c525t-6df1a4e1ab5b92d275978793f3378b1d750e0a3e05c5a24e68a64a05039c65043</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1292467366/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1292467366?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19876399$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Unutmaz, Derya</contributor><creatorcontrib>Lukens, John R</creatorcontrib><creatorcontrib>Dolina, Joseph S</creatorcontrib><creatorcontrib>Kim, Taeg S</creatorcontrib><creatorcontrib>Tacke, Robert S</creatorcontrib><creatorcontrib>Hahn, Young S</creatorcontrib><title>Liver is able to activate naïve CD8+ T cells with dysfunctional anti-viral activity in the murine system</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The liver possesses distinct tolerogenic properties because of continuous exposure to bacterial constituents and nonpathogenic food antigen. The central immune mediators required for the generation of effective immune responses in the liver environment have not been fully elucidated. In this report, we demonstrate that the liver can indeed support effector CD8(+) T cells during adenovirus infection when the T cells are primed in secondary lymphoid tissues. In contrast, when viral antigen is delivered predominantly to the liver via intravenous (IV) adenovirus infection, intrahepatic CD8(+) T cells are significantly impaired in their ability to produce inflammatory cytokines and lyse target cells. Additionally, intrahepatic CD8(+) T cells generated during IV adenovirus infection express elevated levels of PD-1. Notably, lower doses of adenovirus infection do not rescue the impaired effector function of intrahepatic CD8(+) T cell responses. Instead, intrahepatic antigen recognition limits the generation of potent anti-viral responses at both priming and effector stages of the CD8(+) T cell response and accounts for the dysfunctional CD8(+) T cell response observed during IV adenovirus infection. These results also implicate that manipulation of antigen delivery will facilitate the design of improved vaccination strategies to persistent viral infection.</description><subject>Adenoviridae - metabolism</subject><subject>Adenoviridae Infections</subject><subject>Animals</subject><subject>Antiviral agents</subject><subject>Antiviral Agents - chemistry</subject><subject>Bacteria</subject><subject>Bone Marrow Cells - cytology</subject><subject>CD8 antigen</subject><subject>CD8-Positive T-Lymphocytes - immunology</subject><subject>CD8-Positive T-Lymphocytes - metabolism</subject><subject>Cell Differentiation</subject><subject>Coculture Techniques</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Effector cells</subject><subject>Flow Cytometry - methods</subject><subject>Immune response</subject><subject>Immunology/Immune Response</subject><subject>Immunology/Immunity to Infections</subject><subject>Immunology/Immunomodulation</subject><subject>Infections</subject><subject>Inflammation</subject><subject>Intravenous administration</subject><subject>Liver</subject><subject>Liver - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lukens, John R</au><au>Dolina, Joseph S</au><au>Kim, Taeg S</au><au>Tacke, Robert S</au><au>Hahn, Young S</au><au>Unutmaz, Derya</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Liver is able to activate naïve CD8+ T cells with dysfunctional anti-viral activity in the murine system</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2009-10-30</date><risdate>2009</risdate><volume>4</volume><issue>10</issue><spage>e7619</spage><epage>e7619</epage><pages>e7619-e7619</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The liver possesses distinct tolerogenic properties because of continuous exposure to bacterial constituents and nonpathogenic food antigen. The central immune mediators required for the generation of effective immune responses in the liver environment have not been fully elucidated. In this report, we demonstrate that the liver can indeed support effector CD8(+) T cells during adenovirus infection when the T cells are primed in secondary lymphoid tissues. In contrast, when viral antigen is delivered predominantly to the liver via intravenous (IV) adenovirus infection, intrahepatic CD8(+) T cells are significantly impaired in their ability to produce inflammatory cytokines and lyse target cells. Additionally, intrahepatic CD8(+) T cells generated during IV adenovirus infection express elevated levels of PD-1. Notably, lower doses of adenovirus infection do not rescue the impaired effector function of intrahepatic CD8(+) T cell responses. Instead, intrahepatic antigen recognition limits the generation of potent anti-viral responses at both priming and effector stages of the CD8(+) T cell response and accounts for the dysfunctional CD8(+) T cell response observed during IV adenovirus infection. These results also implicate that manipulation of antigen delivery will facilitate the design of improved vaccination strategies to persistent viral infection.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>19876399</pmid><doi>10.1371/journal.pone.0007619</doi><oa>free_for_read</oa></addata></record> |
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subjects | Adenoviridae - metabolism Adenoviridae Infections Animals Antiviral agents Antiviral Agents - chemistry Bacteria Bone Marrow Cells - cytology CD8 antigen CD8-Positive T-Lymphocytes - immunology CD8-Positive T-Lymphocytes - metabolism Cell Differentiation Coculture Techniques Cytokines Cytokines - metabolism Effector cells Flow Cytometry - methods Immune response Immunology/Immune Response Immunology/Immunity to Infections Immunology/Immunomodulation Infections Inflammation Intravenous administration Liver Liver - metabolism Lymphocytes Lymphocytes T Lymphoid tissue Mice Mice, Inbred BALB C Mice, Inbred C57BL Mice, Transgenic PD-1 protein Priming Rodents Spleen - virology T cell receptors Tissues Vaccination Viral infections |
title | Liver is able to activate naïve CD8+ T cells with dysfunctional anti-viral activity in the murine system |
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