Hepatitis C-specific effector and regulatory CD4 T-cell responses are associated with the outcomes of primary infection.
Identifieur interne : 003A36 ( Ncbi/Checkpoint ); précédent : 003A35; suivant : 003A37Hepatitis 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
Affiliations:
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Nguyen</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><wicri:noRegion>NSW</wicri:noRegion></affiliation></author><author><name sortKey="Sugden, P" sort="Sugden, P" uniqKey="Sugden P" first="P" last="Sugden">P. Sugden</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><wicri:noRegion>NSW</wicri:noRegion></affiliation></author><author><name sortKey="Bull, R" sort="Bull, R" uniqKey="Bull R" first="R" last="Bull">R. Bull</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><wicri:noRegion>NSW</wicri:noRegion></affiliation></author><author><name sortKey="Zekry, A" sort="Zekry, A" uniqKey="Zekry A" first="A" last="Zekry">A. 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Seddiki</name><affiliation wicri:level="3"><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><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Créteil</settlement></placeName></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><wicri:noRegion>NSW</wicri:noRegion></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><wicri:noRegion>NSW</wicri:noRegion></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><wicri:noRegion>NSW</wicri:noRegion></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><affiliations><list><country><li>Australie</li><li>France</li></country><region><li>Île-de-France</li></region><settlement><li>Créteil</li></settlement></list><tree><country name="Australie"><noRegion><name sortKey="Keoshkerian, E" sort="Keoshkerian, E" uniqKey="Keoshkerian E" first="E" last="Keoshkerian">E. Keoshkerian</name></noRegion><name sortKey="Bull, R" sort="Bull, R" uniqKey="Bull R" first="R" last="Bull">R. Bull</name><name sortKey="Cameron, B" sort="Cameron, B" uniqKey="Cameron B" first="B" last="Cameron">B. Cameron</name><name sortKey="Hunter, M" sort="Hunter, M" uniqKey="Hunter M" first="M" last="Hunter">M. Hunter</name><name sortKey="Kelleher, A" sort="Kelleher, A" uniqKey="Kelleher A" first="A" last="Kelleher">A. Kelleher</name><name sortKey="Lloyd, A R" sort="Lloyd, A R" uniqKey="Lloyd A" first="A R" last="Lloyd">A R Lloyd</name><name sortKey="Maher, L" sort="Maher, L" uniqKey="Maher L" first="L" last="Maher">L. Maher</name><name sortKey="Nguyen, N" sort="Nguyen, N" uniqKey="Nguyen N" first="N" last="Nguyen">N. Nguyen</name><name sortKey="Sugden, P" sort="Sugden, P" uniqKey="Sugden P" first="P" last="Sugden">P. Sugden</name><name sortKey="Zaunders, J" sort="Zaunders, J" uniqKey="Zaunders J" first="J" last="Zaunders">J. Zaunders</name><name sortKey="Zekry, A" sort="Zekry, A" uniqKey="Zekry A" first="A" last="Zekry">A. Zekry</name></country><country name="France"><region name="Île-de-France"><name sortKey="Seddiki, N" sort="Seddiki, N" uniqKey="Seddiki N" first="N" last="Seddiki">N. Seddiki</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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