Hepatitis C Virus-Induced Myeloid-Derived Suppressor Cells Suppress NK Cell IFN-γ Production by Altering Cellular Metabolism via Arginase-1.
Identifieur interne : 000A94 ( Main/Exploration ); précédent : 000A93; suivant : 000A95Hepatitis C Virus-Induced Myeloid-Derived Suppressor Cells Suppress NK Cell IFN-γ Production by Altering Cellular Metabolism via Arginase-1.
Auteurs : Celeste C. Goh [États-Unis] ; Krystal M. Roggerson [États-Unis] ; Hai-Chon Lee ; Lucy Golden-Mason [États-Unis] ; Hugo R. Rosen [États-Unis] ; Young S. Hahn [États-Unis]Source :
- Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2016.
Descripteurs français
- KwdFr :
- Agranulocytes (immunologie), Agranulocytes (métabolisme), Agranulocytes (virologie), Arginase (métabolisme), Arginine (métabolisme), Cellules cultivées (MeSH), Cellules myéloïdes (immunologie), Cellules myéloïdes (métabolisme), Cellules myéloïdes (virologie), Cellules tueuses naturelles (immunologie), Cellules tueuses naturelles (métabolisme), Hepacivirus (immunologie), Humains (MeSH), Hépatite C (génétique), Hépatite C (immunologie), Hépatite C (métabolisme), Hépatite C (virologie), Interféron gamma (biosynthèse), Lectine-3 de type Ig liant l'acide sialique (métabolisme), Lignée cellulaire (MeSH), Maturation post-transcriptionnelle des ARN (MeSH), Sérine-thréonine kinases TOR (métabolisme), Transduction du signal (MeSH).
- MESH :
- biosynthèse : Interféron gamma.
- génétique : Hépatite C.
- immunologie : Agranulocytes, Cellules myéloïdes, Cellules tueuses naturelles, Hepacivirus, Hépatite C.
- métabolisme : Agranulocytes, Arginase, Arginine, Cellules myéloïdes, Cellules tueuses naturelles, Hépatite C, Lectine-3 de type Ig liant l'acide sialique, Sérine-thréonine kinases TOR.
- virologie : Agranulocytes, Cellules myéloïdes, Hépatite C.
- Cellules cultivées, Humains, Lignée cellulaire, Maturation post-transcriptionnelle des ARN, Transduction du signal.
English descriptors
- KwdEn :
- Arginase (metabolism), Arginine (metabolism), Cell Line (MeSH), Cells, Cultured (MeSH), Hepacivirus (immunology), Hepatitis C (genetics), Hepatitis C (immunology), Hepatitis C (metabolism), Hepatitis C (virology), Humans (MeSH), Interferon-gamma (biosynthesis), Killer Cells, Natural (immunology), Killer Cells, Natural (metabolism), Leukocytes, Mononuclear (immunology), Leukocytes, Mononuclear (metabolism), Leukocytes, Mononuclear (virology), Myeloid Cells (immunology), Myeloid Cells (metabolism), Myeloid Cells (virology), RNA Processing, Post-Transcriptional (MeSH), Sialic Acid Binding Ig-like Lectin 3 (metabolism), Signal Transduction (MeSH), TOR Serine-Threonine Kinases (metabolism).
- MESH :
- chemical , biosynthesis : Interferon-gamma.
- chemical , metabolism : Arginase, Arginine, Sialic Acid Binding Ig-like Lectin 3, TOR Serine-Threonine Kinases.
- genetics : Hepatitis C.
- immunology : Hepacivirus, Hepatitis C, Killer Cells, Natural, Leukocytes, Mononuclear, Myeloid Cells.
- metabolism : Hepatitis C, Killer Cells, Natural, Leukocytes, Mononuclear, Myeloid Cells.
- virology : Hepatitis C, Leukocytes, Mononuclear, Myeloid Cells.
- Cell Line, Cells, Cultured, Humans, RNA Processing, Post-Transcriptional, Signal Transduction.
Abstract
The hepatitis C virus (HCV) infects ∼ 200 million people worldwide. The majority of infected individuals develop persistent infection, resulting in chronic inflammation and liver disease, including cirrhosis and hepatocellular carcinoma. The ability of HCV to establish persistent infection is partly due to its ability to evade the immune response through multiple mechanisms, including suppression of NK cells. NK cells control HCV replication during the early phase of infection and regulate the progression to chronic disease. In particular, IFN-γ produced by NK cells limits viral replication in hepatocytes and is important for the initiation of adaptive immune responses. However, NK cell function is significantly impaired in chronic HCV patients. The cellular and molecular mechanisms responsible for impaired NK cell function in HCV infection are not well defined. In this study, we analyzed the interaction of human NK cells with CD33(+) PBMCs that were exposed to HCV. We found that NK cells cocultured with HCV-conditioned CD33(+) PBMCs produced lower amounts of IFN-γ, with no effect on granzyme B production or cell viability. Importantly, this suppression of NK cell-derived IFN-γ production was mediated by CD33(+)CD11b(lo)HLA-DR(lo) myeloid-derived suppressor cells (MDSCs) via an arginase-1-dependent inhibition of mammalian target of rapamycin activation. Suppression of IFN-γ production was reversed by l-arginine supplementation, consistent with increased MDSC arginase-1 activity. These novel results identify the induction of MDSCs in HCV infection as a potent immune evasion strategy that suppresses antiviral NK cell responses, further indicating that blockade of MDSCs may be a potential therapeutic approach to ameliorate chronic viral infections in the liver.
DOI: 10.4049/jimmunol.1501881
PubMed: 26826241
PubMed Central: PMC4761460
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Goh</name><affiliation wicri:level="2"><nlm:affiliation>Beirne Carter Center for Immunology Research, University of Virginia School of Medicine, Charlottesville, VA 22908; Department of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, VA 22908;</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Virginie</region></placeName><wicri:cityArea>Beirne Carter Center for Immunology Research, University of Virginia School of Medicine, Charlottesville, VA 22908; Department of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville</wicri:cityArea></affiliation></author><author><name sortKey="Roggerson, Krystal M" sort="Roggerson, Krystal M" uniqKey="Roggerson K" first="Krystal M" last="Roggerson">Krystal M. 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Goh</name><affiliation wicri:level="2"><nlm:affiliation>Beirne Carter Center for Immunology Research, University of Virginia School of Medicine, Charlottesville, VA 22908; Department of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, VA 22908;</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Virginie</region></placeName><wicri:cityArea>Beirne Carter Center for Immunology Research, University of Virginia School of Medicine, Charlottesville, VA 22908; Department of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville</wicri:cityArea></affiliation></author><author><name sortKey="Roggerson, Krystal M" sort="Roggerson, Krystal M" uniqKey="Roggerson K" first="Krystal M" last="Roggerson">Krystal M. Roggerson</name><affiliation wicri:level="2"><nlm:affiliation>Beirne Carter Center for Immunology Research, University of Virginia School of Medicine, Charlottesville, VA 22908; Department of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, VA 22908;</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Virginie</region></placeName><wicri:cityArea>Beirne Carter Center for Immunology Research, University of Virginia School of Medicine, Charlottesville, VA 22908; Department of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville</wicri:cityArea></affiliation></author><author><name sortKey="Lee, Hai Chon" sort="Lee, Hai Chon" uniqKey="Lee H" first="Hai-Chon" last="Lee">Hai-Chon Lee</name><affiliation><nlm:affiliation>Beirne Carter Center for Immunology Research, University of Virginia School of Medicine, Charlottesville, VA 22908; Department of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, VA 22908; Wide River Institute of Immunology, Seoul National University, Gangwon 25159, Korea; and.</nlm:affiliation><wicri:noCountry code="subField">Korea; and</wicri:noCountry></affiliation></author><author><name sortKey="Golden Mason, Lucy" sort="Golden Mason, Lucy" uniqKey="Golden Mason L" first="Lucy" last="Golden-Mason">Lucy Golden-Mason</name><affiliation wicri:level="2"><nlm:affiliation>Department of Gastroenterology, University of Colorado Health Sciences Center, Aurora, CO 80045.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Colorado</region></placeName><wicri:cityArea>Department of Gastroenterology, University of Colorado Health Sciences Center, Aurora</wicri:cityArea></affiliation></author><author><name sortKey="Rosen, Hugo R" sort="Rosen, Hugo R" uniqKey="Rosen H" first="Hugo R" last="Rosen">Hugo R. Rosen</name><affiliation wicri:level="2"><nlm:affiliation>Department of Gastroenterology, University of Colorado Health Sciences Center, Aurora, CO 80045.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Colorado</region></placeName><wicri:cityArea>Department of Gastroenterology, University of Colorado Health Sciences Center, Aurora</wicri:cityArea></affiliation></author><author><name sortKey="Hahn, Young S" sort="Hahn, Young S" uniqKey="Hahn Y" first="Young S" last="Hahn">Young S. Hahn</name><affiliation wicri:level="1"><nlm:affiliation>Beirne Carter Center for Immunology Research, University of Virginia School of Medicine, Charlottesville, VA 22908; Department of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, VA 22908; ysh5e@virginia.edu.</nlm:affiliation><country wicri:rule="url">États-Unis</country><wicri:regionArea>Beirne Carter Center for Immunology Research, University of Virginia School of Medicine, Charlottesville, VA 22908; Department of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville</wicri:regionArea><wicri:noRegion>Charlottesville</wicri:noRegion></affiliation></author></analytic><series><title level="j">Journal of immunology (Baltimore, Md. : 1950)</title><idno type="eISSN">1550-6606</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Arginase (metabolism)</term><term>Arginine (metabolism)</term><term>Cell Line (MeSH)</term><term>Cells, Cultured (MeSH)</term><term>Hepacivirus (immunology)</term><term>Hepatitis C (genetics)</term><term>Hepatitis C (immunology)</term><term>Hepatitis C (metabolism)</term><term>Hepatitis C (virology)</term><term>Humans (MeSH)</term><term>Interferon-gamma (biosynthesis)</term><term>Killer Cells, Natural (immunology)</term><term>Killer Cells, Natural (metabolism)</term><term>Leukocytes, Mononuclear (immunology)</term><term>Leukocytes, Mononuclear (metabolism)</term><term>Leukocytes, Mononuclear (virology)</term><term>Myeloid Cells (immunology)</term><term>Myeloid Cells (metabolism)</term><term>Myeloid Cells (virology)</term><term>RNA Processing, Post-Transcriptional (MeSH)</term><term>Sialic Acid Binding Ig-like Lectin 3 (metabolism)</term><term>Signal Transduction (MeSH)</term><term>TOR Serine-Threonine Kinases (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Agranulocytes (immunologie)</term><term>Agranulocytes (métabolisme)</term><term>Agranulocytes (virologie)</term><term>Arginase (métabolisme)</term><term>Arginine (métabolisme)</term><term>Cellules cultivées (MeSH)</term><term>Cellules myéloïdes (immunologie)</term><term>Cellules myéloïdes (métabolisme)</term><term>Cellules myéloïdes (virologie)</term><term>Cellules tueuses naturelles (immunologie)</term><term>Cellules tueuses naturelles (métabolisme)</term><term>Hepacivirus (immunologie)</term><term>Humains (MeSH)</term><term>Hépatite C (génétique)</term><term>Hépatite C (immunologie)</term><term>Hépatite C (métabolisme)</term><term>Hépatite C (virologie)</term><term>Interféron gamma (biosynthèse)</term><term>Lectine-3 de type Ig liant l'acide sialique (métabolisme)</term><term>Lignée cellulaire (MeSH)</term><term>Maturation post-transcriptionnelle des ARN (MeSH)</term><term>Sérine-thréonine kinases TOR (métabolisme)</term><term>Transduction du signal (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Interferon-gamma</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Arginase</term><term>Arginine</term><term>Sialic Acid Binding Ig-like Lectin 3</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Interféron gamma</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Hepatitis C</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Hépatite C</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Agranulocytes</term><term>Cellules myéloïdes</term><term>Cellules tueuses naturelles</term><term>Hepacivirus</term><term>Hépatite C</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Hepacivirus</term><term>Hepatitis C</term><term>Killer Cells, Natural</term><term>Leukocytes, Mononuclear</term><term>Myeloid Cells</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Hepatitis C</term><term>Killer Cells, Natural</term><term>Leukocytes, Mononuclear</term><term>Myeloid Cells</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Agranulocytes</term><term>Arginase</term><term>Arginine</term><term>Cellules myéloïdes</term><term>Cellules tueuses naturelles</term><term>Hépatite C</term><term>Lectine-3 de type Ig liant l'acide sialique</term><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Agranulocytes</term><term>Cellules myéloïdes</term><term>Hépatite C</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Hepatitis C</term><term>Leukocytes, Mononuclear</term><term>Myeloid Cells</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line</term><term>Cells, Cultured</term><term>Humans</term><term>RNA Processing, Post-Transcriptional</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cellules cultivées</term><term>Humains</term><term>Lignée cellulaire</term><term>Maturation post-transcriptionnelle des ARN</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The hepatitis C virus (HCV) infects ∼ 200 million people worldwide. The majority of infected individuals develop persistent infection, resulting in chronic inflammation and liver disease, including cirrhosis and hepatocellular carcinoma. The ability of HCV to establish persistent infection is partly due to its ability to evade the immune response through multiple mechanisms, including suppression of NK cells. NK cells control HCV replication during the early phase of infection and regulate the progression to chronic disease. In particular, IFN-γ produced by NK cells limits viral replication in hepatocytes and is important for the initiation of adaptive immune responses. However, NK cell function is significantly impaired in chronic HCV patients. The cellular and molecular mechanisms responsible for impaired NK cell function in HCV infection are not well defined. In this study, we analyzed the interaction of human NK cells with CD33(+) PBMCs that were exposed to HCV. We found that NK cells cocultured with HCV-conditioned CD33(+) PBMCs produced lower amounts of IFN-γ, with no effect on granzyme B production or cell viability. Importantly, this suppression of NK cell-derived IFN-γ production was mediated by CD33(+)CD11b(lo)HLA-DR(lo) myeloid-derived suppressor cells (MDSCs) via an arginase-1-dependent inhibition of mammalian target of rapamycin activation. Suppression of IFN-γ production was reversed by l-arginine supplementation, consistent with increased MDSC arginase-1 activity. These novel results identify the induction of MDSCs in HCV infection as a potent immune evasion strategy that suppresses antiviral NK cell responses, further indicating that blockade of MDSCs may be a potential therapeutic approach to ameliorate chronic viral infections in the liver.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26826241</PMID><DateCompleted><Year>2016</Year><Month>06</Month><Day>30</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1550-6606</ISSN><JournalIssue CitedMedium="Internet"><Volume>196</Volume><Issue>5</Issue><PubDate><Year>2016</Year><Month>Mar</Month><Day>01</Day></PubDate></JournalIssue><Title>Journal of immunology (Baltimore, Md. : 1950)</Title><ISOAbbreviation>J Immunol</ISOAbbreviation></Journal><ArticleTitle>Hepatitis C Virus-Induced Myeloid-Derived Suppressor Cells Suppress NK Cell IFN-γ Production by Altering Cellular Metabolism via Arginase-1.</ArticleTitle><Pagination><MedlinePgn>2283-92</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.4049/jimmunol.1501881</ELocationID><Abstract><AbstractText>The hepatitis C virus (HCV) infects ∼ 200 million people worldwide. The majority of infected individuals develop persistent infection, resulting in chronic inflammation and liver disease, including cirrhosis and hepatocellular carcinoma. The ability of HCV to establish persistent infection is partly due to its ability to evade the immune response through multiple mechanisms, including suppression of NK cells. NK cells control HCV replication during the early phase of infection and regulate the progression to chronic disease. In particular, IFN-γ produced by NK cells limits viral replication in hepatocytes and is important for the initiation of adaptive immune responses. However, NK cell function is significantly impaired in chronic HCV patients. The cellular and molecular mechanisms responsible for impaired NK cell function in HCV infection are not well defined. In this study, we analyzed the interaction of human NK cells with CD33(+) PBMCs that were exposed to HCV. We found that NK cells cocultured with HCV-conditioned CD33(+) PBMCs produced lower amounts of IFN-γ, with no effect on granzyme B production or cell viability. Importantly, this suppression of NK cell-derived IFN-γ production was mediated by CD33(+)CD11b(lo)HLA-DR(lo) myeloid-derived suppressor cells (MDSCs) via an arginase-1-dependent inhibition of mammalian target of rapamycin activation. Suppression of IFN-γ production was reversed by l-arginine supplementation, consistent with increased MDSC arginase-1 activity. These novel results identify the induction of MDSCs in HCV infection as a potent immune evasion strategy that suppresses antiviral NK cell responses, further indicating that blockade of MDSCs may be a potential therapeutic approach to ameliorate chronic viral infections in the liver.</AbstractText><CopyrightInformation>Copyright © 2016 by The American Association of Immunologists, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Goh</LastName><ForeName>Celeste C</ForeName><Initials>CC</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-0070-3924</Identifier><AffiliationInfo><Affiliation>Beirne Carter Center for Immunology Research, University of Virginia School of Medicine, Charlottesville, VA 22908; Department of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, VA 22908;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Roggerson</LastName><ForeName>Krystal M</ForeName><Initials>KM</Initials><AffiliationInfo><Affiliation>Beirne Carter Center for Immunology Research, University of Virginia School of Medicine, Charlottesville, VA 22908; Department of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, VA 22908;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Hai-Chon</ForeName><Initials>HC</Initials><AffiliationInfo><Affiliation>Beirne Carter Center for Immunology Research, University of Virginia School of Medicine, Charlottesville, VA 22908; Department of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, VA 22908; Wide River Institute of Immunology, Seoul National University, Gangwon 25159, Korea; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Golden-Mason</LastName><ForeName>Lucy</ForeName><Initials>L</Initials><Identifier Source="ORCID">http://orcid.org/0000-0003-3347-4192</Identifier><AffiliationInfo><Affiliation>Department of Gastroenterology, University of Colorado Health Sciences Center, Aurora, CO 80045.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rosen</LastName><ForeName>Hugo R</ForeName><Initials>HR</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-1110-6914</Identifier><AffiliationInfo><Affiliation>Department of Gastroenterology, University of Colorado Health Sciences Center, Aurora, CO 80045.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hahn</LastName><ForeName>Young S</ForeName><Initials>YS</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-2698-9844</Identifier><AffiliationInfo><Affiliation>Beirne Carter Center for Immunology Research, University of Virginia School of Medicine, Charlottesville, VA 22908; Department of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, VA 22908; ysh5e@virginia.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>T32 AI07496</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 AI007496</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>1T34GM105550</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI057591</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 GM008715</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI098126</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 GM08715-14</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI057591</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T34 GM105550</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U19 AI066328</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>01</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J 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Goh</name></region><name sortKey="Golden Mason, Lucy" sort="Golden Mason, Lucy" uniqKey="Golden Mason L" first="Lucy" last="Golden-Mason">Lucy Golden-Mason</name><name sortKey="Hahn, Young S" sort="Hahn, Young S" uniqKey="Hahn Y" first="Young S" last="Hahn">Young S. Hahn</name><name sortKey="Roggerson, Krystal M" sort="Roggerson, Krystal M" uniqKey="Roggerson K" first="Krystal M" last="Roggerson">Krystal M. Roggerson</name><name sortKey="Rosen, Hugo R" sort="Rosen, Hugo R" uniqKey="Rosen H" first="Hugo R" last="Rosen">Hugo R. Rosen</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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