Hepatitis C-specific effector and regulatory CD4 T-cell responses are associated with the outcomes of primary infection.
Identifieur interne : 001434 ( PubMed/Curation ); précédent : 001433; suivant : 001435Hepatitis C-specific effector and regulatory CD4 T-cell responses are associated with the outcomes of primary infection.
Auteurs : E. Keoshkerian [Australie] ; M. Hunter [Australie] ; B. Cameron [Australie] ; N. Nguyen [Australie] ; P. Sugden [Australie] ; R. Bull [Australie] ; A. Zekry [Australie] ; L. Maher [Australie] ; N. Seddiki [France] ; J. Zaunders [Australie] ; A. Kelleher [Australie] ; A R Lloyd [Australie]Source :
- Journal of viral hepatitis [ 1365-2893 ] ; 2016.
Descripteurs français
- KwdFr :
- Adulte, Cytokines (sécrétion), Femelle, Hepacivirus (immunologie), Humains, Hépatite C (immunologie), Lymphocytes T CD4+ (immunologie), Lymphocytes T régulateurs (immunologie), Mâle, Résultat thérapeutique, Sous-populations de lymphocytes T (immunologie), Études longitudinales, Études transversales.
- MESH :
- immunologie : Hepacivirus, Hépatite C, Lymphocytes T CD4+, Lymphocytes T régulateurs, Sous-populations de lymphocytes T.
- sécrétion : Cytokines.
- Adulte, Femelle, Humains, Mâle, Résultat thérapeutique, Études longitudinales, Études transversales.
English descriptors
- KwdEn :
- MESH :
- chemical , secretion : Cytokines.
- immunology : CD4-Positive T-Lymphocytes, Hepacivirus, Hepatitis C, T-Lymphocyte Subsets, T-Lymphocytes, Regulatory.
- Adult, Cross-Sectional Studies, Female, Humans, Longitudinal Studies, Male, Treatment Outcome.
Abstract
Clearance of primary hepatitis C virus (HCV) infection has been associated with strong and broadly targeted cellular immune responses. This study aimed to characterize HCV-specific CD4+ effector and regulatory T-cell numbers and cytokine production during primary infection. Antigen-specific CD4+ T-cell responses were investigated in a longitudinal cohort of subjects from pre-infection to postoutcome, including subjects who cleared [n=12] or became chronically infected [n=17]. A cross-sectional cohort with previously cleared, or chronic infection [n=15 for each], was also studied. Peripheral blood mononuclear cells were incubated with HCV antigens and surface stained for T-effector (CD4+CD25(high) CD134+CD39-) and T-regulatory (CD4+CD25(high) CD134+CD39+) markers, and culture supernatants assayed for cytokine production. Contrary to expectations, the breadth and magnitude of the HCV-specific CD4+ T-cell responses were higher in subjects who became chronically infected. Subjects who cleared the virus had HCV-specific CD4+ T-cell responses dominated by effector T cells and produced higher levels of IFN-γ, in contrast to HCV-specific CD4+ T-cell responses dominated by regulatory T cells and more IL-10 production in those who became chronically infected. Better understanding of the role of antigen-specific CD4+ T-cell responses in primary HCV will further define pathogenesis and help guide development of a preventative vaccine.
DOI: 10.1111/jvh.12576
PubMed: 27558465
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Keoshkerian</name><affiliation wicri:level="1"><nlm:affiliation>UNSW Australia, Kirby Institute (Viral Immunology Systems Program, VISP) and School of Medical Sciences (SOMS), Kensington, NSW, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>UNSW Australia, Kirby Institute (Viral Immunology Systems Program, VISP) and School of Medical Sciences (SOMS), Kensington, NSW</wicri:regionArea></affiliation></author><author><name sortKey="Hunter, M" sort="Hunter, M" uniqKey="Hunter M" first="M" last="Hunter">M. Hunter</name><affiliation wicri:level="1"><nlm:affiliation>UNSW Australia, SOMS (Infection and Immunology Research Centre, IIRC), Kensington, NSW, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>UNSW Australia, SOMS (Infection and Immunology Research Centre, IIRC), Kensington, NSW</wicri:regionArea></affiliation></author><author><name sortKey="Cameron, B" sort="Cameron, B" uniqKey="Cameron B" first="B" last="Cameron">B. Cameron</name><affiliation wicri:level="1"><nlm:affiliation>UNSW Australia, SOMS (Infection and Immunology Research Centre, IIRC), Kensington, NSW, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>UNSW Australia, SOMS (Infection and Immunology Research Centre, IIRC), Kensington, NSW</wicri:regionArea></affiliation></author><author><name sortKey="Nguyen, N" sort="Nguyen, N" uniqKey="Nguyen N" first="N" last="Nguyen">N. 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Maher</name><affiliation wicri:level="1"><nlm:affiliation>UNSW Australia, Kirby Institute (Viral Hepatitis Epidemiology and Prevention Program VHEPP), Kensington, NSW, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>UNSW Australia, Kirby Institute (Viral Hepatitis Epidemiology and Prevention Program VHEPP), Kensington, NSW</wicri:regionArea></affiliation></author><author><name sortKey="Seddiki, N" sort="Seddiki, N" uniqKey="Seddiki N" first="N" last="Seddiki">N. Seddiki</name><affiliation wicri:level="1"><nlm:affiliation>The Vaccine Research Institute (VRI), INSERM, Créteil, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>The Vaccine Research Institute (VRI), INSERM, Créteil</wicri:regionArea></affiliation></author><author><name sortKey="Zaunders, J" sort="Zaunders, J" uniqKey="Zaunders J" first="J" last="Zaunders">J. Zaunders</name><affiliation wicri:level="1"><nlm:affiliation>UNSW Australia, Kirby Institute (Immunovirology and Pathogenesis Program, IVPP), Kensington, NSW, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>UNSW Australia, Kirby Institute (Immunovirology and Pathogenesis Program, IVPP), Kensington, NSW</wicri:regionArea></affiliation></author><author><name sortKey="Kelleher, A" sort="Kelleher, A" uniqKey="Kelleher A" first="A" last="Kelleher">A. Kelleher</name><affiliation wicri:level="1"><nlm:affiliation>UNSW Australia, Kirby Institute (Immunovirology and Pathogenesis Program, IVPP), Kensington, NSW, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>UNSW Australia, Kirby Institute (Immunovirology and Pathogenesis Program, IVPP), Kensington, NSW</wicri:regionArea></affiliation></author><author><name sortKey="Lloyd, A R" sort="Lloyd, A R" uniqKey="Lloyd A" first="A R" last="Lloyd">A R Lloyd</name><affiliation wicri:level="1"><nlm:affiliation>UNSW Australia, Kirby Institute (Viral Immunology Systems Program, VISP) and School of Medical Sciences (SOMS), Kensington, NSW, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>UNSW Australia, Kirby Institute (Viral Immunology Systems Program, VISP) and School of Medical Sciences (SOMS), Kensington, NSW</wicri:regionArea></affiliation></author></analytic><series><title level="j">Journal of viral hepatitis</title><idno type="eISSN">1365-2893</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>CD4-Positive T-Lymphocytes (immunology)</term><term>Cross-Sectional Studies</term><term>Cytokines (secretion)</term><term>Female</term><term>Hepacivirus (immunology)</term><term>Hepatitis C (immunology)</term><term>Humans</term><term>Longitudinal Studies</term><term>Male</term><term>T-Lymphocyte Subsets (immunology)</term><term>T-Lymphocytes, Regulatory (immunology)</term><term>Treatment Outcome</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adulte</term><term>Cytokines (sécrétion)</term><term>Femelle</term><term>Hepacivirus (immunologie)</term><term>Humains</term><term>Hépatite C (immunologie)</term><term>Lymphocytes T CD4+ (immunologie)</term><term>Lymphocytes T régulateurs (immunologie)</term><term>Mâle</term><term>Résultat thérapeutique</term><term>Sous-populations de lymphocytes T (immunologie)</term><term>Études longitudinales</term><term>Études transversales</term></keywords><keywords scheme="MESH" type="chemical" qualifier="secretion" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Hepacivirus</term><term>Hépatite C</term><term>Lymphocytes T CD4+</term><term>Lymphocytes T régulateurs</term><term>Sous-populations de lymphocytes T</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>CD4-Positive T-Lymphocytes</term><term>Hepacivirus</term><term>Hepatitis C</term><term>T-Lymphocyte Subsets</term><term>T-Lymphocytes, Regulatory</term></keywords><keywords scheme="MESH" qualifier="sécrétion" xml:lang="fr"><term>Cytokines</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Cross-Sectional Studies</term><term>Female</term><term>Humans</term><term>Longitudinal Studies</term><term>Male</term><term>Treatment Outcome</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adulte</term><term>Femelle</term><term>Humains</term><term>Mâle</term><term>Résultat thérapeutique</term><term>Études longitudinales</term><term>Études transversales</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Clearance of primary hepatitis C virus (HCV) infection has been associated with strong and broadly targeted cellular immune responses. This study aimed to characterize HCV-specific CD4+ effector and regulatory T-cell numbers and cytokine production during primary infection. Antigen-specific CD4+ T-cell responses were investigated in a longitudinal cohort of subjects from pre-infection to postoutcome, including subjects who cleared [n=12] or became chronically infected [n=17]. A cross-sectional cohort with previously cleared, or chronic infection [n=15 for each], was also studied. Peripheral blood mononuclear cells were incubated with HCV antigens and surface stained for T-effector (CD4+CD25(high) CD134+CD39-) and T-regulatory (CD4+CD25(high) CD134+CD39+) markers, and culture supernatants assayed for cytokine production. Contrary to expectations, the breadth and magnitude of the HCV-specific CD4+ T-cell responses were higher in subjects who became chronically infected. Subjects who cleared the virus had HCV-specific CD4+ T-cell responses dominated by effector T cells and produced higher levels of IFN-γ, in contrast to HCV-specific CD4+ T-cell responses dominated by regulatory T cells and more IL-10 production in those who became chronically infected. Better understanding of the role of antigen-specific CD4+ T-cell responses in primary HCV will further define pathogenesis and help guide development of a preventative vaccine.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27558465</PMID><DateCreated><Year>2016</Year><Month>08</Month><Day>25</Day></DateCreated><DateCompleted><Year>2017</Year><Month>10</Month><Day>30</Day></DateCompleted><DateRevised><Year>2017</Year><Month>10</Month><Day>30</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1365-2893</ISSN><JournalIssue CitedMedium="Internet"><Volume>23</Volume><Issue>12</Issue><PubDate><Year>2016</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Journal of viral hepatitis</Title><ISOAbbreviation>J. Viral Hepat.</ISOAbbreviation></Journal><ArticleTitle>Hepatitis C-specific effector and regulatory CD4 T-cell responses are associated with the outcomes of primary infection.</ArticleTitle><Pagination><MedlinePgn>985-993</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/jvh.12576</ELocationID><Abstract><AbstractText>Clearance of primary hepatitis C virus (HCV) infection has been associated with strong and broadly targeted cellular immune responses. This study aimed to characterize HCV-specific CD4+ effector and regulatory T-cell numbers and cytokine production during primary infection. Antigen-specific CD4+ T-cell responses were investigated in a longitudinal cohort of subjects from pre-infection to postoutcome, including subjects who cleared [n=12] or became chronically infected [n=17]. A cross-sectional cohort with previously cleared, or chronic infection [n=15 for each], was also studied. Peripheral blood mononuclear cells were incubated with HCV antigens and surface stained for T-effector (CD4+CD25(high) CD134+CD39-) and T-regulatory (CD4+CD25(high) CD134+CD39+) markers, and culture supernatants assayed for cytokine production. Contrary to expectations, the breadth and magnitude of the HCV-specific CD4+ T-cell responses were higher in subjects who became chronically infected. Subjects who cleared the virus had HCV-specific CD4+ T-cell responses dominated by effector T cells and produced higher levels of IFN-γ, in contrast to HCV-specific CD4+ T-cell responses dominated by regulatory T cells and more IL-10 production in those who became chronically infected. Better understanding of the role of antigen-specific CD4+ T-cell responses in primary HCV will further define pathogenesis and help guide development of a preventative vaccine.</AbstractText><CopyrightInformation>© 2016 John Wiley & Sons Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Keoshkerian</LastName><ForeName>E</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>UNSW Australia, Kirby Institute (Viral Immunology Systems Program, VISP) and School of Medical Sciences (SOMS), Kensington, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hunter</LastName><ForeName>M</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>UNSW Australia, SOMS (Infection and Immunology Research Centre, IIRC), Kensington, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cameron</LastName><ForeName>B</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>UNSW Australia, SOMS (Infection and Immunology Research Centre, IIRC), Kensington, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nguyen</LastName><ForeName>N</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>UNSW Australia, SOMS (Infection and Immunology Research Centre, IIRC), Kensington, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sugden</LastName><ForeName>P</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>UNSW Australia, SOMS (Infection and Immunology Research Centre, IIRC), Kensington, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bull</LastName><ForeName>R</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>UNSW Australia, Kirby Institute (Viral Immunology Systems Program, VISP) and School of Medical Sciences (SOMS), Kensington, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zekry</LastName><ForeName>A</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>UNSW Australia, St George and Sutherland Clinical School, Sydney, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Maher</LastName><ForeName>L</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>UNSW Australia, Kirby Institute (Viral Hepatitis Epidemiology and Prevention Program VHEPP), Kensington, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Seddiki</LastName><ForeName>N</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>The Vaccine Research Institute (VRI), INSERM, Créteil, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zaunders</LastName><ForeName>J</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>UNSW Australia, Kirby Institute (Immunovirology and Pathogenesis Program, IVPP), Kensington, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kelleher</LastName><ForeName>A</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>UNSW Australia, Kirby Institute (Immunovirology and Pathogenesis Program, IVPP), Kensington, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lloyd</LastName><ForeName>A R</ForeName><Initials>AR</Initials><AffiliationInfo><Affiliation>UNSW Australia, Kirby Institute (Viral Immunology Systems Program, VISP) and School of Medical Sciences (SOMS), Kensington, NSW, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><CollectiveName>HITS-p and HITS-c investigators</CollectiveName></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>08</Month><Day>25</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Viral Hepat</MedlineTA><NlmUniqueID>9435672</NlmUniqueID><ISSNLinking>1352-0504</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015496" MajorTopicYN="N">CD4-Positive T-Lymphocytes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003430" MajorTopicYN="N">Cross-Sectional Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000557" MajorTopicYN="N">secretion</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016174" MajorTopicYN="N">Hepacivirus</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006526" MajorTopicYN="N">Hepatitis C</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008137" MajorTopicYN="N">Longitudinal Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016176" MajorTopicYN="N">T-Lymphocyte Subsets</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050378" MajorTopicYN="N">T-Lymphocytes, Regulatory</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">T effectors</Keyword><Keyword MajorTopicYN="N">T regulatory cells</Keyword><Keyword MajorTopicYN="N">acute hepatitis C</Keyword><Keyword MajorTopicYN="N">antigen-specific CD4 T cells</Keyword><Keyword MajorTopicYN="N">cytokines</Keyword></KeywordList><InvestigatorList><Investigator ValidYN="Y"><LastName>Dolan</LastName><ForeName>Kate</ForeName><Initials>K</Initials></Investigator><Investigator ValidYN="Y"><LastName>Haber</LastName><ForeName>Paul</ForeName><Initials>P</Initials></Investigator><Investigator ValidYN="Y"><LastName>Rawlinson</LastName><ForeName>William</ForeName><Initials>W</Initials></Investigator><Investigator ValidYN="Y"><LastName>Treloar</LastName><ForeName>Carla</ForeName><Initials>C</Initials></Investigator><Investigator ValidYN="Y"><LastName>Dore</LastName><ForeName>Greg</ForeName><Initials>G</Initials></Investigator><Investigator ValidYN="Y"><LastName>Luciani</LastName><ForeName>Fabio</ForeName><Initials>F</Initials></Investigator></InvestigatorList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>02</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>06</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>8</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>10</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>8</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27558465</ArticleId><ArticleId IdType="doi">10.1111/jvh.12576</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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