PD-1/PDL1 and CD28/CD80 pathways modulate natural killer T cell function to inhibit hepatitis B virus replication
Summary α‐Galactosylceramide (α‐GalCer)‐activated natural killer T (NKT) cells have antiviral properties against hepatitis B virus (HBV). However, α‐GalCer activation of NKT cells can induce anergy. We hypothesized that this effect may be overcome by a treatment strategy that includes manipulation o...
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| Veröffentlicht in: | Journal of viral hepatitis 2013-04, Vol.20 (s1), p.27-39 |
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| creator | Wang, X. F. Lei, Y. Chen, M. Chen, C. B. Ren, H. Shi, T. D. |
| description | Summary
α‐Galactosylceramide (α‐GalCer)‐activated natural killer T (NKT) cells have antiviral properties against hepatitis B virus (HBV). However, α‐GalCer activation of NKT cells can induce anergy. We hypothesized that this effect may be overcome by a treatment strategy that includes manipulation of CD28/CD80 costimulatory and PD‐1/PDL1 coinhibitory signals of NKT cells, thereby enhancing the anti‐HBV effect of α‐GalCer. We established a transgenic mouse model of chronic HBV infection and investigated hepatic NKT cell frequencies, functions and expression of immunomodulatory factors. Our results showed that compared with uninfected control mice, hepatic NKT cells from HBV transgenic mice displayed lower frequencies (7.91% vs 16.74%, P |
| doi_str_mv | 10.1111/jvh.12061 |
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α‐Galactosylceramide (α‐GalCer)‐activated natural killer T (NKT) cells have antiviral properties against hepatitis B virus (HBV). However, α‐GalCer activation of NKT cells can induce anergy. We hypothesized that this effect may be overcome by a treatment strategy that includes manipulation of CD28/CD80 costimulatory and PD‐1/PDL1 coinhibitory signals of NKT cells, thereby enhancing the anti‐HBV effect of α‐GalCer. We established a transgenic mouse model of chronic HBV infection and investigated hepatic NKT cell frequencies, functions and expression of immunomodulatory factors. Our results showed that compared with uninfected control mice, hepatic NKT cells from HBV transgenic mice displayed lower frequencies (7.91% vs 16.74%, P < 0.05), impaired capabilities to produce interferon (IFN)‐γ (5.6% vs 1.4%, P < 0.05) and interleukin (IL)‐4 (6.8% vs 0.3%, P < 0.05), higher expression of PD‐1 (9.64% vs 6.36%, P < 0.05) and lower expression of CD28 (5.05% vs 28.88%, P < 0.05). However, when hepatic mononuclear cells (MNCs) were isolated from HBV transgenic mice, α‐GalCer exposure in culture remarkably upregulated both PD‐1+ NKT cells (P < 0.05) and CD28+ NKT cells (P < 0.05). Furthermore, when HBV transgenic mice were treated with combination therapies consisting of α‐GalCer and anti‐PDL1 monoclonal antibody (mAb) and/or anti‐CD80/anti‐CD28 mAbs, IFN‐γ+ NKT cell frequency was selectively increased (P < 0.05) and HBV replication was suppressed; these effects were accompanied by varying degrees and types of liver damage. Surprisingly, activating CD28/CD80 signal in HBV transgenic mice was more effective but caused less liver injury than blocking PD‐1/PDL1 signal in modulating αGalCer‐activated NKT cell function to inhibit HBV infection. Our findings also show that combined therapy with blocking PD‐1/PDL1 and activating CD28/CD80 signal in the presence of aGalCer cannot superimpose the effect of antivirus. α‐GalCer combination therapy that modulates the CD28/CD80 pathways of NKT cells may represent a promising approach to inhibit HBV replication in chronically infected patients.]]></description><identifier>ISSN: 1352-0504</identifier><identifier>EISSN: 1365-2893</identifier><identifier>DOI: 10.1111/jvh.12061</identifier><identifier>PMID: 23458522</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Anergy ; Animal models ; Animals ; Antibodies, Monoclonal - administration & dosage ; Antibodies, Monoclonal - immunology ; Antiviral activity ; B7-1 Antigen - immunology ; B7-1 Antigen - metabolism ; B7-H1 Antigen - immunology ; B7-H1 Antigen - metabolism ; CD28 antigen ; CD28 Antigens - immunology ; CD28 Antigens - metabolism ; CD28/CD80 ; CD80 antigen ; Cell culture ; China ; Chronic infection ; Disease Models, Animal ; Female ; Flow Cytometry ; galactosylceramide ; Galactosylceramides - administration & dosage ; Galactosylceramides - immunology ; Galactosylceramides - pharmacology ; gamma -Interferon ; Hepatitis B virus ; Hepatitis B virus - drug effects ; Hepatitis B virus - genetics ; Hepatitis B virus - physiology ; Hepatitis B, Chronic - drug therapy ; Hepatitis B, Chronic - immunology ; Hepatitis B, Chronic - virology ; Humans ; Immunomodulation ; Injuries ; Interferon ; Interleukins ; Leukocytes (mononuclear) ; Liver ; Lymphocyte Activation ; Lymphocytes T ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Monoclonal antibodies ; Natural killer cells ; natural killer T cell ; Natural Killer T-Cells - immunology ; Natural Killer T-Cells - metabolism ; PD-1 protein ; PD1/PDL1 ; Programmed Cell Death 1 Receptor - immunology ; Programmed Cell Death 1 Receptor - metabolism ; Receptors, Immunologic - immunology ; Receptors, Immunologic - metabolism ; Replication ; Transgenic mice ; Treatment Outcome ; Virus Replication - immunology</subject><ispartof>Journal of viral hepatitis, 2013-04, Vol.20 (s1), p.27-39</ispartof><rights>2012 Blackwell Publishing Ltd</rights><rights>2012 Blackwell Publishing Ltd.</rights><rights>Copyright © 2013 Blackwell Publishing Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fjvh.12061$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fjvh.12061$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,27923,27924,45573,45574</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23458522$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, X. F.</creatorcontrib><creatorcontrib>Lei, Y.</creatorcontrib><creatorcontrib>Chen, M.</creatorcontrib><creatorcontrib>Chen, C. B.</creatorcontrib><creatorcontrib>Ren, H.</creatorcontrib><creatorcontrib>Shi, T. D.</creatorcontrib><title>PD-1/PDL1 and CD28/CD80 pathways modulate natural killer T cell function to inhibit hepatitis B virus replication</title><title>Journal of viral hepatitis</title><addtitle>J Viral Hepat</addtitle><description><![CDATA[Summary
α‐Galactosylceramide (α‐GalCer)‐activated natural killer T (NKT) cells have antiviral properties against hepatitis B virus (HBV). However, α‐GalCer activation of NKT cells can induce anergy. We hypothesized that this effect may be overcome by a treatment strategy that includes manipulation of CD28/CD80 costimulatory and PD‐1/PDL1 coinhibitory signals of NKT cells, thereby enhancing the anti‐HBV effect of α‐GalCer. We established a transgenic mouse model of chronic HBV infection and investigated hepatic NKT cell frequencies, functions and expression of immunomodulatory factors. Our results showed that compared with uninfected control mice, hepatic NKT cells from HBV transgenic mice displayed lower frequencies (7.91% vs 16.74%, P < 0.05), impaired capabilities to produce interferon (IFN)‐γ (5.6% vs 1.4%, P < 0.05) and interleukin (IL)‐4 (6.8% vs 0.3%, P < 0.05), higher expression of PD‐1 (9.64% vs 6.36%, P < 0.05) and lower expression of CD28 (5.05% vs 28.88%, P < 0.05). However, when hepatic mononuclear cells (MNCs) were isolated from HBV transgenic mice, α‐GalCer exposure in culture remarkably upregulated both PD‐1+ NKT cells (P < 0.05) and CD28+ NKT cells (P < 0.05). Furthermore, when HBV transgenic mice were treated with combination therapies consisting of α‐GalCer and anti‐PDL1 monoclonal antibody (mAb) and/or anti‐CD80/anti‐CD28 mAbs, IFN‐γ+ NKT cell frequency was selectively increased (P < 0.05) and HBV replication was suppressed; these effects were accompanied by varying degrees and types of liver damage. Surprisingly, activating CD28/CD80 signal in HBV transgenic mice was more effective but caused less liver injury than blocking PD‐1/PDL1 signal in modulating αGalCer‐activated NKT cell function to inhibit HBV infection. Our findings also show that combined therapy with blocking PD‐1/PDL1 and activating CD28/CD80 signal in the presence of aGalCer cannot superimpose the effect of antivirus. α‐GalCer combination therapy that modulates the CD28/CD80 pathways of NKT cells may represent a promising approach to inhibit HBV replication in chronically infected patients.]]></description><subject>Anergy</subject><subject>Animal models</subject><subject>Animals</subject><subject>Antibodies, Monoclonal - administration & dosage</subject><subject>Antibodies, Monoclonal - immunology</subject><subject>Antiviral activity</subject><subject>B7-1 Antigen - immunology</subject><subject>B7-1 Antigen - metabolism</subject><subject>B7-H1 Antigen - immunology</subject><subject>B7-H1 Antigen - metabolism</subject><subject>CD28 antigen</subject><subject>CD28 Antigens - immunology</subject><subject>CD28 Antigens - metabolism</subject><subject>CD28/CD80</subject><subject>CD80 antigen</subject><subject>Cell culture</subject><subject>China</subject><subject>Chronic infection</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Flow Cytometry</subject><subject>galactosylceramide</subject><subject>Galactosylceramides - administration & dosage</subject><subject>Galactosylceramides - immunology</subject><subject>Galactosylceramides - pharmacology</subject><subject>gamma -Interferon</subject><subject>Hepatitis B virus</subject><subject>Hepatitis B virus - drug effects</subject><subject>Hepatitis B virus - genetics</subject><subject>Hepatitis B virus - physiology</subject><subject>Hepatitis B, Chronic - drug therapy</subject><subject>Hepatitis B, Chronic - immunology</subject><subject>Hepatitis B, Chronic - virology</subject><subject>Humans</subject><subject>Immunomodulation</subject><subject>Injuries</subject><subject>Interferon</subject><subject>Interleukins</subject><subject>Leukocytes (mononuclear)</subject><subject>Liver</subject><subject>Lymphocyte Activation</subject><subject>Lymphocytes T</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Monoclonal antibodies</subject><subject>Natural killer cells</subject><subject>natural killer T cell</subject><subject>Natural Killer T-Cells - immunology</subject><subject>Natural Killer T-Cells - metabolism</subject><subject>PD-1 protein</subject><subject>PD1/PDL1</subject><subject>Programmed Cell Death 1 Receptor - immunology</subject><subject>Programmed Cell Death 1 Receptor - metabolism</subject><subject>Receptors, Immunologic - immunology</subject><subject>Receptors, Immunologic - metabolism</subject><subject>Replication</subject><subject>Transgenic mice</subject><subject>Treatment Outcome</subject><subject>Virus Replication - immunology</subject><issn>1352-0504</issn><issn>1365-2893</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU1v1DAQhi0EoqVw4A8gS1x6SdfjrzhH2EALXUEPK5C4WE7i1XrrTba207L_Hqfb9tATc5mR5nlHM_Mi9B7IGeSYbW7XZ0CJhBfoGJgUBVUVeznVghZEEH6E3sS4IQQYFfAaHVHGhRKUHqObq7qA2VW9AGz6Ds9rqmbzWhG8M2l9Z_YRb4du9CZZ3Js0BuPxtfPeBrzErfUer8a-TW7ocRqw69eucQmvbVa75CL-jG9dGCMOduddaybwLXq1Mj7adw_5BC2_flnOL4rFz_Nv80-LwjFBoBAGuOKms1AClyupiAIGRHa86lQlBZNNC6JhpWE230IaZYAysEJy1pqOnaDTw9hdGG5GG5PeujhtbHo7jFHnV7CyqgSI_0Ch5KQipMzox2foZhhDn-84UBVj1UR9eKDGZms7vQtua8JeP749A7MDcOe83T_1gejJT5391Pd-6u-_Lu6LrCgOCheT_fukMOFay5KVQv_-ca7VH84v60uuFfsHoMSc1A</recordid><startdate>201304</startdate><enddate>201304</enddate><creator>Wang, X. F.</creator><creator>Lei, Y.</creator><creator>Chen, M.</creator><creator>Chen, C. B.</creator><creator>Ren, H.</creator><creator>Shi, T. D.</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201304</creationdate><title>PD-1/PDL1 and CD28/CD80 pathways modulate natural killer T cell function to inhibit hepatitis B virus replication</title><author>Wang, X. F. ; Lei, Y. ; Chen, M. ; Chen, C. B. ; Ren, H. ; Shi, T. D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i3501-5a1484ade17146f680813106d49d896536bc15b37a3e5850b8a1231e5643cad3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Anergy</topic><topic>Animal models</topic><topic>Animals</topic><topic>Antibodies, Monoclonal - administration & dosage</topic><topic>Antibodies, Monoclonal - immunology</topic><topic>Antiviral activity</topic><topic>B7-1 Antigen - immunology</topic><topic>B7-1 Antigen - metabolism</topic><topic>B7-H1 Antigen - immunology</topic><topic>B7-H1 Antigen - metabolism</topic><topic>CD28 antigen</topic><topic>CD28 Antigens - immunology</topic><topic>CD28 Antigens - metabolism</topic><topic>CD28/CD80</topic><topic>CD80 antigen</topic><topic>Cell culture</topic><topic>China</topic><topic>Chronic infection</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Flow Cytometry</topic><topic>galactosylceramide</topic><topic>Galactosylceramides - administration & dosage</topic><topic>Galactosylceramides - immunology</topic><topic>Galactosylceramides - pharmacology</topic><topic>gamma -Interferon</topic><topic>Hepatitis B virus</topic><topic>Hepatitis B virus - drug effects</topic><topic>Hepatitis B virus - genetics</topic><topic>Hepatitis B virus - physiology</topic><topic>Hepatitis B, Chronic - drug therapy</topic><topic>Hepatitis B, Chronic - immunology</topic><topic>Hepatitis B, Chronic - virology</topic><topic>Humans</topic><topic>Immunomodulation</topic><topic>Injuries</topic><topic>Interferon</topic><topic>Interleukins</topic><topic>Leukocytes (mononuclear)</topic><topic>Liver</topic><topic>Lymphocyte Activation</topic><topic>Lymphocytes T</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Monoclonal antibodies</topic><topic>Natural killer cells</topic><topic>natural killer T cell</topic><topic>Natural Killer T-Cells - immunology</topic><topic>Natural Killer T-Cells - metabolism</topic><topic>PD-1 protein</topic><topic>PD1/PDL1</topic><topic>Programmed Cell Death 1 Receptor - immunology</topic><topic>Programmed Cell Death 1 Receptor - metabolism</topic><topic>Receptors, Immunologic - immunology</topic><topic>Receptors, Immunologic - metabolism</topic><topic>Replication</topic><topic>Transgenic mice</topic><topic>Treatment Outcome</topic><topic>Virus Replication - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, X. F.</creatorcontrib><creatorcontrib>Lei, Y.</creatorcontrib><creatorcontrib>Chen, M.</creatorcontrib><creatorcontrib>Chen, C. B.</creatorcontrib><creatorcontrib>Ren, H.</creatorcontrib><creatorcontrib>Shi, T. D.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of viral hepatitis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, X. F.</au><au>Lei, Y.</au><au>Chen, M.</au><au>Chen, C. B.</au><au>Ren, H.</au><au>Shi, T. D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PD-1/PDL1 and CD28/CD80 pathways modulate natural killer T cell function to inhibit hepatitis B virus replication</atitle><jtitle>Journal of viral hepatitis</jtitle><addtitle>J Viral Hepat</addtitle><date>2013-04</date><risdate>2013</risdate><volume>20</volume><issue>s1</issue><spage>27</spage><epage>39</epage><pages>27-39</pages><issn>1352-0504</issn><eissn>1365-2893</eissn><abstract><![CDATA[Summary
α‐Galactosylceramide (α‐GalCer)‐activated natural killer T (NKT) cells have antiviral properties against hepatitis B virus (HBV). However, α‐GalCer activation of NKT cells can induce anergy. We hypothesized that this effect may be overcome by a treatment strategy that includes manipulation of CD28/CD80 costimulatory and PD‐1/PDL1 coinhibitory signals of NKT cells, thereby enhancing the anti‐HBV effect of α‐GalCer. We established a transgenic mouse model of chronic HBV infection and investigated hepatic NKT cell frequencies, functions and expression of immunomodulatory factors. Our results showed that compared with uninfected control mice, hepatic NKT cells from HBV transgenic mice displayed lower frequencies (7.91% vs 16.74%, P < 0.05), impaired capabilities to produce interferon (IFN)‐γ (5.6% vs 1.4%, P < 0.05) and interleukin (IL)‐4 (6.8% vs 0.3%, P < 0.05), higher expression of PD‐1 (9.64% vs 6.36%, P < 0.05) and lower expression of CD28 (5.05% vs 28.88%, P < 0.05). However, when hepatic mononuclear cells (MNCs) were isolated from HBV transgenic mice, α‐GalCer exposure in culture remarkably upregulated both PD‐1+ NKT cells (P < 0.05) and CD28+ NKT cells (P < 0.05). Furthermore, when HBV transgenic mice were treated with combination therapies consisting of α‐GalCer and anti‐PDL1 monoclonal antibody (mAb) and/or anti‐CD80/anti‐CD28 mAbs, IFN‐γ+ NKT cell frequency was selectively increased (P < 0.05) and HBV replication was suppressed; these effects were accompanied by varying degrees and types of liver damage. Surprisingly, activating CD28/CD80 signal in HBV transgenic mice was more effective but caused less liver injury than blocking PD‐1/PDL1 signal in modulating αGalCer‐activated NKT cell function to inhibit HBV infection. Our findings also show that combined therapy with blocking PD‐1/PDL1 and activating CD28/CD80 signal in the presence of aGalCer cannot superimpose the effect of antivirus. α‐GalCer combination therapy that modulates the CD28/CD80 pathways of NKT cells may represent a promising approach to inhibit HBV replication in chronically infected patients.]]></abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>23458522</pmid><doi>10.1111/jvh.12061</doi><tpages>13</tpages></addata></record> |
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| subjects | Anergy Animal models Animals Antibodies, Monoclonal - administration & dosage Antibodies, Monoclonal - immunology Antiviral activity B7-1 Antigen - immunology B7-1 Antigen - metabolism B7-H1 Antigen - immunology B7-H1 Antigen - metabolism CD28 antigen CD28 Antigens - immunology CD28 Antigens - metabolism CD28/CD80 CD80 antigen Cell culture China Chronic infection Disease Models, Animal Female Flow Cytometry galactosylceramide Galactosylceramides - administration & dosage Galactosylceramides - immunology Galactosylceramides - pharmacology gamma -Interferon Hepatitis B virus Hepatitis B virus - drug effects Hepatitis B virus - genetics Hepatitis B virus - physiology Hepatitis B, Chronic - drug therapy Hepatitis B, Chronic - immunology Hepatitis B, Chronic - virology Humans Immunomodulation Injuries Interferon Interleukins Leukocytes (mononuclear) Liver Lymphocyte Activation Lymphocytes T Mice Mice, Inbred C57BL Mice, Transgenic Monoclonal antibodies Natural killer cells natural killer T cell Natural Killer T-Cells - immunology Natural Killer T-Cells - metabolism PD-1 protein PD1/PDL1 Programmed Cell Death 1 Receptor - immunology Programmed Cell Death 1 Receptor - metabolism Receptors, Immunologic - immunology Receptors, Immunologic - metabolism Replication Transgenic mice Treatment Outcome Virus Replication - immunology |
| title | PD-1/PDL1 and CD28/CD80 pathways modulate natural killer T cell function to inhibit hepatitis B virus replication |
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