Tumor necrosis factor-alpha induced by hepatitis B virus core mediating the immune response for hepatitis B viral clearance in mice model
Persistent hepatitis B viral (HBV) infection results in chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma (HCC). An efficient control of virus infections requires the coordinated actions of both innate and adaptive immune responses. In order to define the role of innate immunity effec...
Gespeichert in:
| Veröffentlicht in: | PloS one 2014-07, Vol.9 (7), p.e103008-e103008 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | e103008 |
|---|---|
| container_issue | 7 |
| container_start_page | e103008 |
| container_title | PloS one |
| container_volume | 9 |
| creator | Tzeng, Horng-Tay Tsai, Hwei-Fang Chyuan, I-Tsu Liao, Hsiu-Jung Chen, Chun-Jen Chen, Pei-Jer Hsu, Ping-Ning |
| description | Persistent hepatitis B viral (HBV) infection results in chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma (HCC). An efficient control of virus infections requires the coordinated actions of both innate and adaptive immune responses. In order to define the role of innate immunity effectors against HBV, viral clearance was studied in a panel of immunodeficient mouse strains by the hydrodynamic injection approach. Our results demonstrate that HBV viral clearance is not changed in IFN-α/β receptor (IFNAR), RIG-I, MDA5, MYD88, NLRP3, ASC, and IL-1R knock-out mice, indicating that these innate immunity effectors are not required for HBV clearance. In contrast, HBV persists in the absence of tumor necrosis factor-alpha (TNF-α) or in mice treated with the soluble TNF receptor blocker, Etanercept. In these mice, there was an increase in PD-1-expressing CD8+ T-cells and an increase of serum HBV DNA, HBV core, and surface antigen expression as well as viral replication within the liver. Furthermore, the induction of TNF-α in clearing HBV is dependent on the HBV core, and TNF blockage eliminated HBV core-induced viral clearance effects. Finally, the intra-hepatic leukocytes (IHLs), but not the hepatocytes, are the cell source responsible for TNF-α production induced by HBcAg. These results provide evidences for TNF-α mediated innate immune mechanisms in HBV clearance and explain the mechanism of HBV reactivation during therapy with TNF blockage agents. |
| doi_str_mv | 10.1371/journal.pone.0103008 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_plos_</sourceid><recordid>TN_cdi_plos_journals_1547308548</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A418139147</galeid><doaj_id>oai_doaj_org_article_940a9464b1fb41329913ff0a1e449f14</doaj_id><sourcerecordid>A418139147</sourcerecordid><originalsourceid>FETCH-LOGICAL-c758t-3cc8f8d3f100c56fdc22a275494c63bba6e39cb7b6d0bacc184005d6a802c0b3</originalsourceid><addsrcrecordid>eNqNk99q2zAUxs3YWLtsbzA2wWBsF8kkS3bkm0FX9idQKGxht0KWpVjBllJJLusj7K130rglLr0YvpA5-p1POp_OybLXBC8IXZJPWz8EJ7vFzju9wARTjPmT7JRUNJ-XOaZPj_5PshcxbjEuKC_L59lJXmC25Lg6zf6uh94H5LQKPtqIjFTJh7nsdq1E1jWD0g2qb1CrdzLZBMQXdG3DEJHyQaNeNxbiboNSq5Ht-8FpFHSES0WNDCg_SJQdUp2WQToFvEO9hbX3je5eZs-M7KJ-Na6zbP3t6_r8x_zi8vvq_OxirpYFT3OqFDe8oYZgrIrSNCrPZb4sWMVUSetalppWql7WZYNrqRThDOpuSslxrnBNZ9nbg-yu81GMJkZBCrakmBeMA7E6EI2XW7ELtpfhRnhpxW3Ah42QIVkoQ1QMy4qVrCamZoTmVUWoMVgSzVhlCAOtz-NpQw1eKe0SWDARne4424qNvxaM4ILlBAQ-jALBXw06JtHbqHTXSaf9cHtvXtK8ICWg7x6gj1c3UhsJBVhnPJyr9qLijBFOaEWAnWWLRyj4Gg0vBh1nLMQnCR8nCcAk_Sdt5BCjWP36-f_s5e8p-_6IbbXsUht9NyQLHTYF2QHcN3IM2tybTLDYD8ydG2I_MGIcGEh7c_xA90l3E0L_AelqEZY</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1547308548</pqid></control><display><type>article</type><title>Tumor necrosis factor-alpha induced by hepatitis B virus core mediating the immune response for hepatitis B viral clearance in mice model</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><source>Public Library of Science (PLoS)</source><creator>Tzeng, Horng-Tay ; Tsai, Hwei-Fang ; Chyuan, I-Tsu ; Liao, Hsiu-Jung ; Chen, Chun-Jen ; Chen, Pei-Jer ; Hsu, Ping-Ning</creator><creatorcontrib>Tzeng, Horng-Tay ; Tsai, Hwei-Fang ; Chyuan, I-Tsu ; Liao, Hsiu-Jung ; Chen, Chun-Jen ; Chen, Pei-Jer ; Hsu, Ping-Ning</creatorcontrib><description>Persistent hepatitis B viral (HBV) infection results in chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma (HCC). An efficient control of virus infections requires the coordinated actions of both innate and adaptive immune responses. In order to define the role of innate immunity effectors against HBV, viral clearance was studied in a panel of immunodeficient mouse strains by the hydrodynamic injection approach. Our results demonstrate that HBV viral clearance is not changed in IFN-α/β receptor (IFNAR), RIG-I, MDA5, MYD88, NLRP3, ASC, and IL-1R knock-out mice, indicating that these innate immunity effectors are not required for HBV clearance. In contrast, HBV persists in the absence of tumor necrosis factor-alpha (TNF-α) or in mice treated with the soluble TNF receptor blocker, Etanercept. In these mice, there was an increase in PD-1-expressing CD8+ T-cells and an increase of serum HBV DNA, HBV core, and surface antigen expression as well as viral replication within the liver. Furthermore, the induction of TNF-α in clearing HBV is dependent on the HBV core, and TNF blockage eliminated HBV core-induced viral clearance effects. Finally, the intra-hepatic leukocytes (IHLs), but not the hepatocytes, are the cell source responsible for TNF-α production induced by HBcAg. These results provide evidences for TNF-α mediated innate immune mechanisms in HBV clearance and explain the mechanism of HBV reactivation during therapy with TNF blockage agents.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0103008</identifier><identifier>PMID: 25047809</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Activation ; Adaptive immunity ; Animals ; Biology and Life Sciences ; Blockage ; CD8 antigen ; Chronic infection ; Cirrhosis ; Deoxyribonucleic acid ; Disease Models, Animal ; DNA ; Effectors ; Etanercept ; Gene expression ; Health aspects ; Hepatitis ; Hepatitis B ; Hepatitis B Core Antigens - metabolism ; Hepatitis B virus - immunology ; Hepatocellular carcinoma ; Hepatocytes ; Immune clearance ; Immune response ; Immune system ; Immunity ; Immunity, Innate ; Immunodeficiency ; Infection ; Innate immunity ; Interferon ; Interleukin 1 receptors ; Leukocytes ; Liver ; Liver - immunology ; Liver - metabolism ; Liver cancer ; Liver cirrhosis ; Lymphocytes T ; Medicine and Health Sciences ; Mice ; MyD88 protein ; Necrosis ; PD-1 protein ; Rodents ; T cells ; Tumor necrosis factor ; Tumor necrosis factor receptors ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Tumors ; Virus Replication - immunology ; Viruses ; α-Interferon</subject><ispartof>PloS one, 2014-07, Vol.9 (7), p.e103008-e103008</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Tzeng et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://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. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Tzeng et al 2014 Tzeng et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-3cc8f8d3f100c56fdc22a275494c63bba6e39cb7b6d0bacc184005d6a802c0b3</citedby><cites>FETCH-LOGICAL-c758t-3cc8f8d3f100c56fdc22a275494c63bba6e39cb7b6d0bacc184005d6a802c0b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4105421/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4105421/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25047809$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tzeng, Horng-Tay</creatorcontrib><creatorcontrib>Tsai, Hwei-Fang</creatorcontrib><creatorcontrib>Chyuan, I-Tsu</creatorcontrib><creatorcontrib>Liao, Hsiu-Jung</creatorcontrib><creatorcontrib>Chen, Chun-Jen</creatorcontrib><creatorcontrib>Chen, Pei-Jer</creatorcontrib><creatorcontrib>Hsu, Ping-Ning</creatorcontrib><title>Tumor necrosis factor-alpha induced by hepatitis B virus core mediating the immune response for hepatitis B viral clearance in mice model</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Persistent hepatitis B viral (HBV) infection results in chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma (HCC). An efficient control of virus infections requires the coordinated actions of both innate and adaptive immune responses. In order to define the role of innate immunity effectors against HBV, viral clearance was studied in a panel of immunodeficient mouse strains by the hydrodynamic injection approach. Our results demonstrate that HBV viral clearance is not changed in IFN-α/β receptor (IFNAR), RIG-I, MDA5, MYD88, NLRP3, ASC, and IL-1R knock-out mice, indicating that these innate immunity effectors are not required for HBV clearance. In contrast, HBV persists in the absence of tumor necrosis factor-alpha (TNF-α) or in mice treated with the soluble TNF receptor blocker, Etanercept. In these mice, there was an increase in PD-1-expressing CD8+ T-cells and an increase of serum HBV DNA, HBV core, and surface antigen expression as well as viral replication within the liver. Furthermore, the induction of TNF-α in clearing HBV is dependent on the HBV core, and TNF blockage eliminated HBV core-induced viral clearance effects. Finally, the intra-hepatic leukocytes (IHLs), but not the hepatocytes, are the cell source responsible for TNF-α production induced by HBcAg. These results provide evidences for TNF-α mediated innate immune mechanisms in HBV clearance and explain the mechanism of HBV reactivation during therapy with TNF blockage agents.</description><subject>Activation</subject><subject>Adaptive immunity</subject><subject>Animals</subject><subject>Biology and Life Sciences</subject><subject>Blockage</subject><subject>CD8 antigen</subject><subject>Chronic infection</subject><subject>Cirrhosis</subject><subject>Deoxyribonucleic acid</subject><subject>Disease Models, Animal</subject><subject>DNA</subject><subject>Effectors</subject><subject>Etanercept</subject><subject>Gene expression</subject><subject>Health aspects</subject><subject>Hepatitis</subject><subject>Hepatitis B</subject><subject>Hepatitis B Core Antigens - metabolism</subject><subject>Hepatitis B virus - immunology</subject><subject>Hepatocellular carcinoma</subject><subject>Hepatocytes</subject><subject>Immune clearance</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Immunity</subject><subject>Immunity, Innate</subject><subject>Immunodeficiency</subject><subject>Infection</subject><subject>Innate immunity</subject><subject>Interferon</subject><subject>Interleukin 1 receptors</subject><subject>Leukocytes</subject><subject>Liver</subject><subject>Liver - immunology</subject><subject>Liver - metabolism</subject><subject>Liver cancer</subject><subject>Liver cirrhosis</subject><subject>Lymphocytes T</subject><subject>Medicine and Health Sciences</subject><subject>Mice</subject><subject>MyD88 protein</subject><subject>Necrosis</subject><subject>PD-1 protein</subject><subject>Rodents</subject><subject>T cells</subject><subject>Tumor necrosis factor</subject><subject>Tumor necrosis factor receptors</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Tumors</subject><subject>Virus Replication - immunology</subject><subject>Viruses</subject><subject>α-Interferon</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk99q2zAUxs3YWLtsbzA2wWBsF8kkS3bkm0FX9idQKGxht0KWpVjBllJJLusj7K130rglLr0YvpA5-p1POp_OybLXBC8IXZJPWz8EJ7vFzju9wARTjPmT7JRUNJ-XOaZPj_5PshcxbjEuKC_L59lJXmC25Lg6zf6uh94H5LQKPtqIjFTJh7nsdq1E1jWD0g2qb1CrdzLZBMQXdG3DEJHyQaNeNxbiboNSq5Ht-8FpFHSES0WNDCg_SJQdUp2WQToFvEO9hbX3je5eZs-M7KJ-Na6zbP3t6_r8x_zi8vvq_OxirpYFT3OqFDe8oYZgrIrSNCrPZb4sWMVUSetalppWql7WZYNrqRThDOpuSslxrnBNZ9nbg-yu81GMJkZBCrakmBeMA7E6EI2XW7ELtpfhRnhpxW3Ah42QIVkoQ1QMy4qVrCamZoTmVUWoMVgSzVhlCAOtz-NpQw1eKe0SWDARne4424qNvxaM4ILlBAQ-jALBXw06JtHbqHTXSaf9cHtvXtK8ICWg7x6gj1c3UhsJBVhnPJyr9qLijBFOaEWAnWWLRyj4Gg0vBh1nLMQnCR8nCcAk_Sdt5BCjWP36-f_s5e8p-_6IbbXsUht9NyQLHTYF2QHcN3IM2tybTLDYD8ydG2I_MGIcGEh7c_xA90l3E0L_AelqEZY</recordid><startdate>20140721</startdate><enddate>20140721</enddate><creator>Tzeng, Horng-Tay</creator><creator>Tsai, Hwei-Fang</creator><creator>Chyuan, I-Tsu</creator><creator>Liao, Hsiu-Jung</creator><creator>Chen, Chun-Jen</creator><creator>Chen, Pei-Jer</creator><creator>Hsu, Ping-Ning</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140721</creationdate><title>Tumor necrosis factor-alpha induced by hepatitis B virus core mediating the immune response for hepatitis B viral clearance in mice model</title><author>Tzeng, Horng-Tay ; Tsai, Hwei-Fang ; Chyuan, I-Tsu ; Liao, Hsiu-Jung ; Chen, Chun-Jen ; Chen, Pei-Jer ; Hsu, Ping-Ning</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-3cc8f8d3f100c56fdc22a275494c63bba6e39cb7b6d0bacc184005d6a802c0b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Activation</topic><topic>Adaptive immunity</topic><topic>Animals</topic><topic>Biology and Life Sciences</topic><topic>Blockage</topic><topic>CD8 antigen</topic><topic>Chronic infection</topic><topic>Cirrhosis</topic><topic>Deoxyribonucleic acid</topic><topic>Disease Models, Animal</topic><topic>DNA</topic><topic>Effectors</topic><topic>Etanercept</topic><topic>Gene expression</topic><topic>Health aspects</topic><topic>Hepatitis</topic><topic>Hepatitis B</topic><topic>Hepatitis B Core Antigens - metabolism</topic><topic>Hepatitis B virus - immunology</topic><topic>Hepatocellular carcinoma</topic><topic>Hepatocytes</topic><topic>Immune clearance</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Immunity</topic><topic>Immunity, Innate</topic><topic>Immunodeficiency</topic><topic>Infection</topic><topic>Innate immunity</topic><topic>Interferon</topic><topic>Interleukin 1 receptors</topic><topic>Leukocytes</topic><topic>Liver</topic><topic>Liver - immunology</topic><topic>Liver - metabolism</topic><topic>Liver cancer</topic><topic>Liver cirrhosis</topic><topic>Lymphocytes T</topic><topic>Medicine and Health Sciences</topic><topic>Mice</topic><topic>MyD88 protein</topic><topic>Necrosis</topic><topic>PD-1 protein</topic><topic>Rodents</topic><topic>T cells</topic><topic>Tumor necrosis factor</topic><topic>Tumor necrosis factor receptors</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><topic>Tumors</topic><topic>Virus Replication - immunology</topic><topic>Viruses</topic><topic>α-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tzeng, Horng-Tay</creatorcontrib><creatorcontrib>Tsai, Hwei-Fang</creatorcontrib><creatorcontrib>Chyuan, I-Tsu</creatorcontrib><creatorcontrib>Liao, Hsiu-Jung</creatorcontrib><creatorcontrib>Chen, Chun-Jen</creatorcontrib><creatorcontrib>Chen, Pei-Jer</creatorcontrib><creatorcontrib>Hsu, Ping-Ning</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - 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>Tzeng, Horng-Tay</au><au>Tsai, Hwei-Fang</au><au>Chyuan, I-Tsu</au><au>Liao, Hsiu-Jung</au><au>Chen, Chun-Jen</au><au>Chen, Pei-Jer</au><au>Hsu, Ping-Ning</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tumor necrosis factor-alpha induced by hepatitis B virus core mediating the immune response for hepatitis B viral clearance in mice model</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-07-21</date><risdate>2014</risdate><volume>9</volume><issue>7</issue><spage>e103008</spage><epage>e103008</epage><pages>e103008-e103008</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Persistent hepatitis B viral (HBV) infection results in chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma (HCC). An efficient control of virus infections requires the coordinated actions of both innate and adaptive immune responses. In order to define the role of innate immunity effectors against HBV, viral clearance was studied in a panel of immunodeficient mouse strains by the hydrodynamic injection approach. Our results demonstrate that HBV viral clearance is not changed in IFN-α/β receptor (IFNAR), RIG-I, MDA5, MYD88, NLRP3, ASC, and IL-1R knock-out mice, indicating that these innate immunity effectors are not required for HBV clearance. In contrast, HBV persists in the absence of tumor necrosis factor-alpha (TNF-α) or in mice treated with the soluble TNF receptor blocker, Etanercept. In these mice, there was an increase in PD-1-expressing CD8+ T-cells and an increase of serum HBV DNA, HBV core, and surface antigen expression as well as viral replication within the liver. Furthermore, the induction of TNF-α in clearing HBV is dependent on the HBV core, and TNF blockage eliminated HBV core-induced viral clearance effects. Finally, the intra-hepatic leukocytes (IHLs), but not the hepatocytes, are the cell source responsible for TNF-α production induced by HBcAg. These results provide evidences for TNF-α mediated innate immune mechanisms in HBV clearance and explain the mechanism of HBV reactivation during therapy with TNF blockage agents.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25047809</pmid><doi>10.1371/journal.pone.0103008</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2014-07, Vol.9 (7), p.e103008-e103008 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1547308548 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Activation Adaptive immunity Animals Biology and Life Sciences Blockage CD8 antigen Chronic infection Cirrhosis Deoxyribonucleic acid Disease Models, Animal DNA Effectors Etanercept Gene expression Health aspects Hepatitis Hepatitis B Hepatitis B Core Antigens - metabolism Hepatitis B virus - immunology Hepatocellular carcinoma Hepatocytes Immune clearance Immune response Immune system Immunity Immunity, Innate Immunodeficiency Infection Innate immunity Interferon Interleukin 1 receptors Leukocytes Liver Liver - immunology Liver - metabolism Liver cancer Liver cirrhosis Lymphocytes T Medicine and Health Sciences Mice MyD88 protein Necrosis PD-1 protein Rodents T cells Tumor necrosis factor Tumor necrosis factor receptors Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-TNF Tumor necrosis factor-α Tumors Virus Replication - immunology Viruses α-Interferon |
| title | Tumor necrosis factor-alpha induced by hepatitis B virus core mediating the immune response for hepatitis B viral clearance in mice model |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-08T14%3A28%3A51IST&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=Tumor%20necrosis%20factor-alpha%20induced%20by%20hepatitis%20B%20virus%20core%20mediating%20the%20immune%20response%20for%20hepatitis%20B%20viral%20clearance%20in%20mice%20model&rft.jtitle=PloS%20one&rft.au=Tzeng,%20Horng-Tay&rft.date=2014-07-21&rft.volume=9&rft.issue=7&rft.spage=e103008&rft.epage=e103008&rft.pages=e103008-e103008&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0103008&rft_dat=%3Cgale_plos_%3EA418139147%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=1547308548&rft_id=info:pmid/25047809&rft_galeid=A418139147&rft_doaj_id=oai_doaj_org_article_940a9464b1fb41329913ff0a1e449f14&rfr_iscdi=true |