HBV vaccination and HBV infection induces HBV-specific natural killer cell memory
ObjectiveVaccination against hepatitis B virus (HBV) confers protection from subsequent infection through immunological memory that is traditionally considered the domain of the adaptive immune system. This view has been challenged following the identification of antigen-specific memory natural kill...
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| Veröffentlicht in: | Gut 2021-02, Vol.70 (2), p.357-369 |
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| creator | Wijaya, Ratna S Read, Scott A Truong, Naomi R Han, Shuanglin Chen, Dishen Shahidipour, Haleh Fewings, Nicole L Schibeci, Stephen Azardaryany, Mahmoud K Parnell, Grant P Booth, David van der Poorten, David Lin, Rita George, Jacob Douglas, Mark W Ahlenstiel, Golo |
| description | ObjectiveVaccination against hepatitis B virus (HBV) confers protection from subsequent infection through immunological memory that is traditionally considered the domain of the adaptive immune system. This view has been challenged following the identification of antigen-specific memory natural killer cells (mNKs) in mice and non-human primates. While the presence of mNKs has been suggested in humans based on the expansion of NK cells following pathogen exposure, evidence regarding antigen-specificity is lacking. Here, we demonstrate the existence of HBV-specific mNKs in humans after vaccination and in chronic HBV infection.DesignNK cell responses were evaluated by flow cytometry and ELISA following challenge with HBV antigens in HBV vaccinated, non-vaccinated and chronic HBV-infected individuals.ResultsNK cells from vaccinated subjects demonstrated higher cytotoxic and proliferative responses against autologous hepatitis B surface antigen (HBsAg)-pulsed monocyte-derived dendritic cells (moDCs) compared with unvaccinated subjects. Moreover, NK cell lysis of HBsAg-pulsed moDCs was significantly higher than that of hepatitis B core antigen (HBcAg)-pulsed moDCs (non-vaccine antigen) or tumour necrosis factor α-activated moDCs in a NKG2D-dependent manner. The mNKs response was mediated by CD56dim NK cells coexpressing CD57, CD69 and KLRG1. Further, mNKs from chronic hepatitis B patients exhibited greater degranulation against HBcAg-pulsed moDCs compared with unvaccinated or vaccinated patients. Notably, mNK activity was negatively correlated with HBV DNA levels.ConclusionsOur data support the presence of a mature mNKs following HBV antigen exposure either through vaccination or infection. Harnessing these antigen specific, functionally active mNKs provides an opportunity to develop novel treatments targeting HBV in chronic infection. |
| doi_str_mv | 10.1136/gutjnl-2019-319252 |
| format | Article |
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This view has been challenged following the identification of antigen-specific memory natural killer cells (mNKs) in mice and non-human primates. While the presence of mNKs has been suggested in humans based on the expansion of NK cells following pathogen exposure, evidence regarding antigen-specificity is lacking. Here, we demonstrate the existence of HBV-specific mNKs in humans after vaccination and in chronic HBV infection.DesignNK cell responses were evaluated by flow cytometry and ELISA following challenge with HBV antigens in HBV vaccinated, non-vaccinated and chronic HBV-infected individuals.ResultsNK cells from vaccinated subjects demonstrated higher cytotoxic and proliferative responses against autologous hepatitis B surface antigen (HBsAg)-pulsed monocyte-derived dendritic cells (moDCs) compared with unvaccinated subjects. Moreover, NK cell lysis of HBsAg-pulsed moDCs was significantly higher than that of hepatitis B core antigen (HBcAg)-pulsed moDCs (non-vaccine antigen) or tumour necrosis factor α-activated moDCs in a NKG2D-dependent manner. The mNKs response was mediated by CD56dim NK cells coexpressing CD57, CD69 and KLRG1. Further, mNKs from chronic hepatitis B patients exhibited greater degranulation against HBcAg-pulsed moDCs compared with unvaccinated or vaccinated patients. Notably, mNK activity was negatively correlated with HBV DNA levels.ConclusionsOur data support the presence of a mature mNKs following HBV antigen exposure either through vaccination or infection. Harnessing these antigen specific, functionally active mNKs provides an opportunity to develop novel treatments targeting HBV in chronic infection.</description><identifier>ISSN: 0017-5749</identifier><identifier>EISSN: 1468-3288</identifier><identifier>DOI: 10.1136/gutjnl-2019-319252</identifier><identifier>PMID: 32229546</identifier><language>eng</language><publisher>England: BMJ Publishing Group Ltd and British Society of Gastroenterology</publisher><subject>Antigens ; CD57 antigen ; CD69 antigen ; cellular immunity ; Chronic infection ; chronic viral hepatitis ; Cloning ; Core protein ; Cytokines ; Cytotoxicity ; Degranulation ; Dendritic cells ; Dimensional analysis ; Enzyme-linked immunosorbent assay ; Flow cytometry ; Hepatitis B ; Hepatitis B core antigen ; Hepatitis B surface antigen ; Hepatology ; immune response ; Immune system ; Immunological memory ; Immunology ; Infections ; KLRG1 protein ; Lymphocytes ; Lysis ; Monocytes ; Natural killer cells ; NKG2 antigen ; Software ; Tumor necrosis factor ; Tumors ; Vaccination ; Vaccines ; Viral infections ; Viruses</subject><ispartof>Gut, 2021-02, Vol.70 (2), p.357-369</ispartof><rights>Author(s) (or their employer(s)) 2021. No commercial re-use. See rights and permissions. Published by BMJ.</rights><rights>2021 Author(s) (or their employer(s)) 2021. No commercial re-use. See rights and permissions. Published by BMJ.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b474t-6ce743aedea5de5af3878fb44de4316dfb10dc398f229588b5ee8e48ab978d8f3</citedby><cites>FETCH-LOGICAL-b474t-6ce743aedea5de5af3878fb44de4316dfb10dc398f229588b5ee8e48ab978d8f3</cites><orcidid>0000-0003-0026-1457 ; 0000-0001-6775-2061 ; 0000-0002-9011-4014 ; 0000-0002-8421-5476</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32229546$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wijaya, Ratna S</creatorcontrib><creatorcontrib>Read, Scott A</creatorcontrib><creatorcontrib>Truong, Naomi R</creatorcontrib><creatorcontrib>Han, Shuanglin</creatorcontrib><creatorcontrib>Chen, Dishen</creatorcontrib><creatorcontrib>Shahidipour, Haleh</creatorcontrib><creatorcontrib>Fewings, Nicole L</creatorcontrib><creatorcontrib>Schibeci, Stephen</creatorcontrib><creatorcontrib>Azardaryany, Mahmoud K</creatorcontrib><creatorcontrib>Parnell, Grant P</creatorcontrib><creatorcontrib>Booth, David</creatorcontrib><creatorcontrib>van der Poorten, David</creatorcontrib><creatorcontrib>Lin, Rita</creatorcontrib><creatorcontrib>George, Jacob</creatorcontrib><creatorcontrib>Douglas, Mark W</creatorcontrib><creatorcontrib>Ahlenstiel, Golo</creatorcontrib><title>HBV vaccination and HBV infection induces HBV-specific natural killer cell memory</title><title>Gut</title><addtitle>Gut</addtitle><addtitle>Gut</addtitle><description>ObjectiveVaccination against hepatitis B virus (HBV) confers protection from subsequent infection through immunological memory that is traditionally considered the domain of the adaptive immune system. This view has been challenged following the identification of antigen-specific memory natural killer cells (mNKs) in mice and non-human primates. While the presence of mNKs has been suggested in humans based on the expansion of NK cells following pathogen exposure, evidence regarding antigen-specificity is lacking. Here, we demonstrate the existence of HBV-specific mNKs in humans after vaccination and in chronic HBV infection.DesignNK cell responses were evaluated by flow cytometry and ELISA following challenge with HBV antigens in HBV vaccinated, non-vaccinated and chronic HBV-infected individuals.ResultsNK cells from vaccinated subjects demonstrated higher cytotoxic and proliferative responses against autologous hepatitis B surface antigen (HBsAg)-pulsed monocyte-derived dendritic cells (moDCs) compared with unvaccinated subjects. Moreover, NK cell lysis of HBsAg-pulsed moDCs was significantly higher than that of hepatitis B core antigen (HBcAg)-pulsed moDCs (non-vaccine antigen) or tumour necrosis factor α-activated moDCs in a NKG2D-dependent manner. The mNKs response was mediated by CD56dim NK cells coexpressing CD57, CD69 and KLRG1. Further, mNKs from chronic hepatitis B patients exhibited greater degranulation against HBcAg-pulsed moDCs compared with unvaccinated or vaccinated patients. Notably, mNK activity was negatively correlated with HBV DNA levels.ConclusionsOur data support the presence of a mature mNKs following HBV antigen exposure either through vaccination or infection. Harnessing these antigen specific, functionally active mNKs provides an opportunity to develop novel treatments targeting HBV in chronic infection.</description><subject>Antigens</subject><subject>CD57 antigen</subject><subject>CD69 antigen</subject><subject>cellular immunity</subject><subject>Chronic infection</subject><subject>chronic viral hepatitis</subject><subject>Cloning</subject><subject>Core protein</subject><subject>Cytokines</subject><subject>Cytotoxicity</subject><subject>Degranulation</subject><subject>Dendritic cells</subject><subject>Dimensional analysis</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Flow cytometry</subject><subject>Hepatitis B</subject><subject>Hepatitis B core antigen</subject><subject>Hepatitis B surface antigen</subject><subject>Hepatology</subject><subject>immune response</subject><subject>Immune system</subject><subject>Immunological memory</subject><subject>Immunology</subject><subject>Infections</subject><subject>KLRG1 protein</subject><subject>Lymphocytes</subject><subject>Lysis</subject><subject>Monocytes</subject><subject>Natural killer cells</subject><subject>NKG2 antigen</subject><subject>Software</subject><subject>Tumor necrosis factor</subject><subject>Tumors</subject><subject>Vaccination</subject><subject>Vaccines</subject><subject>Viral 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vaccination and HBV infection induces HBV-specific natural killer cell memory</title><author>Wijaya, Ratna S ; Read, Scott A ; Truong, Naomi R ; Han, Shuanglin ; Chen, Dishen ; Shahidipour, Haleh ; Fewings, Nicole L ; Schibeci, Stephen ; Azardaryany, Mahmoud K ; Parnell, Grant P ; Booth, David ; van der Poorten, David ; Lin, Rita ; George, Jacob ; Douglas, Mark W ; Ahlenstiel, Golo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b474t-6ce743aedea5de5af3878fb44de4316dfb10dc398f229588b5ee8e48ab978d8f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Antigens</topic><topic>CD57 antigen</topic><topic>CD69 antigen</topic><topic>cellular immunity</topic><topic>Chronic infection</topic><topic>chronic viral hepatitis</topic><topic>Cloning</topic><topic>Core protein</topic><topic>Cytokines</topic><topic>Cytotoxicity</topic><topic>Degranulation</topic><topic>Dendritic cells</topic><topic>Dimensional analysis</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Flow cytometry</topic><topic>Hepatitis B</topic><topic>Hepatitis B core antigen</topic><topic>Hepatitis B surface antigen</topic><topic>Hepatology</topic><topic>immune response</topic><topic>Immune system</topic><topic>Immunological memory</topic><topic>Immunology</topic><topic>Infections</topic><topic>KLRG1 protein</topic><topic>Lymphocytes</topic><topic>Lysis</topic><topic>Monocytes</topic><topic>Natural killer cells</topic><topic>NKG2 antigen</topic><topic>Software</topic><topic>Tumor necrosis factor</topic><topic>Tumors</topic><topic>Vaccination</topic><topic>Vaccines</topic><topic>Viral infections</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wijaya, Ratna S</creatorcontrib><creatorcontrib>Read, Scott A</creatorcontrib><creatorcontrib>Truong, Naomi R</creatorcontrib><creatorcontrib>Han, 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Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science 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>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Gut</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wijaya, Ratna S</au><au>Read, Scott A</au><au>Truong, Naomi R</au><au>Han, Shuanglin</au><au>Chen, Dishen</au><au>Shahidipour, Haleh</au><au>Fewings, Nicole L</au><au>Schibeci, Stephen</au><au>Azardaryany, Mahmoud K</au><au>Parnell, Grant P</au><au>Booth, David</au><au>van der Poorten, David</au><au>Lin, Rita</au><au>George, Jacob</au><au>Douglas, Mark W</au><au>Ahlenstiel, Golo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HBV vaccination and HBV infection induces HBV-specific natural killer cell memory</atitle><jtitle>Gut</jtitle><stitle>Gut</stitle><addtitle>Gut</addtitle><date>2021-02-01</date><risdate>2021</risdate><volume>70</volume><issue>2</issue><spage>357</spage><epage>369</epage><pages>357-369</pages><issn>0017-5749</issn><eissn>1468-3288</eissn><abstract>ObjectiveVaccination against hepatitis B virus (HBV) confers protection from subsequent infection through immunological memory that is traditionally considered the domain of the adaptive immune system. This view has been challenged following the identification of antigen-specific memory natural killer cells (mNKs) in mice and non-human primates. While the presence of mNKs has been suggested in humans based on the expansion of NK cells following pathogen exposure, evidence regarding antigen-specificity is lacking. Here, we demonstrate the existence of HBV-specific mNKs in humans after vaccination and in chronic HBV infection.DesignNK cell responses were evaluated by flow cytometry and ELISA following challenge with HBV antigens in HBV vaccinated, non-vaccinated and chronic HBV-infected individuals.ResultsNK cells from vaccinated subjects demonstrated higher cytotoxic and proliferative responses against autologous hepatitis B surface antigen (HBsAg)-pulsed monocyte-derived dendritic cells (moDCs) compared with unvaccinated subjects. Moreover, NK cell lysis of HBsAg-pulsed moDCs was significantly higher than that of hepatitis B core antigen (HBcAg)-pulsed moDCs (non-vaccine antigen) or tumour necrosis factor α-activated moDCs in a NKG2D-dependent manner. The mNKs response was mediated by CD56dim NK cells coexpressing CD57, CD69 and KLRG1. Further, mNKs from chronic hepatitis B patients exhibited greater degranulation against HBcAg-pulsed moDCs compared with unvaccinated or vaccinated patients. Notably, mNK activity was negatively correlated with HBV DNA levels.ConclusionsOur data support the presence of a mature mNKs following HBV antigen exposure either through vaccination or infection. Harnessing these antigen specific, functionally active mNKs provides an opportunity to develop novel treatments targeting HBV in chronic infection.</abstract><cop>England</cop><pub>BMJ Publishing Group Ltd and British Society of Gastroenterology</pub><pmid>32229546</pmid><doi>10.1136/gutjnl-2019-319252</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0003-0026-1457</orcidid><orcidid>https://orcid.org/0000-0001-6775-2061</orcidid><orcidid>https://orcid.org/0000-0002-9011-4014</orcidid><orcidid>https://orcid.org/0000-0002-8421-5476</orcidid></addata></record> |
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| subjects | Antigens CD57 antigen CD69 antigen cellular immunity Chronic infection chronic viral hepatitis Cloning Core protein Cytokines Cytotoxicity Degranulation Dendritic cells Dimensional analysis Enzyme-linked immunosorbent assay Flow cytometry Hepatitis B Hepatitis B core antigen Hepatitis B surface antigen Hepatology immune response Immune system Immunological memory Immunology Infections KLRG1 protein Lymphocytes Lysis Monocytes Natural killer cells NKG2 antigen Software Tumor necrosis factor Tumors Vaccination Vaccines Viral infections Viruses |
| title | HBV vaccination and HBV infection induces HBV-specific natural killer cell memory |
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