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Cytomegalovirus Infection : A Driving Force in Human T Cell Immunosenescence: A Driving Force in Human T Cell Immunosenescence
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Zeitschriftentitel: | Annals of the New York Academy of Sciences |
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Personen und Körperschaften: | , , , , , , , , , |
In: | Annals of the New York Academy of Sciences, 1114, 2007, 1, S. 23-35 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
Wiley
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Schlagwörter: |
author_facet |
KOCH, SVEN LARBI, ANIS ÖZCELIK, DENNIS SOLANA, RAFAEL GOUTTEFANGEAS, CÉCILE ATTIG, SEBASTIAN WIKBY, ANDERS STRINDHALL, JAN FRANCESCHI, CLAUDIO PAWELEC, GRAHAM KOCH, SVEN LARBI, ANIS ÖZCELIK, DENNIS SOLANA, RAFAEL GOUTTEFANGEAS, CÉCILE ATTIG, SEBASTIAN WIKBY, ANDERS STRINDHALL, JAN FRANCESCHI, CLAUDIO PAWELEC, GRAHAM |
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author |
KOCH, SVEN LARBI, ANIS ÖZCELIK, DENNIS SOLANA, RAFAEL GOUTTEFANGEAS, CÉCILE ATTIG, SEBASTIAN WIKBY, ANDERS STRINDHALL, JAN FRANCESCHI, CLAUDIO PAWELEC, GRAHAM |
spellingShingle |
KOCH, SVEN LARBI, ANIS ÖZCELIK, DENNIS SOLANA, RAFAEL GOUTTEFANGEAS, CÉCILE ATTIG, SEBASTIAN WIKBY, ANDERS STRINDHALL, JAN FRANCESCHI, CLAUDIO PAWELEC, GRAHAM Annals of the New York Academy of Sciences Cytomegalovirus Infection : A Driving Force in Human T Cell Immunosenescence History and Philosophy of Science General Biochemistry, Genetics and Molecular Biology General Neuroscience |
author_sort |
koch, sven |
spelling |
KOCH, SVEN LARBI, ANIS ÖZCELIK, DENNIS SOLANA, RAFAEL GOUTTEFANGEAS, CÉCILE ATTIG, SEBASTIAN WIKBY, ANDERS STRINDHALL, JAN FRANCESCHI, CLAUDIO PAWELEC, GRAHAM 0077-8923 1749-6632 Wiley History and Philosophy of Science General Biochemistry, Genetics and Molecular Biology General Neuroscience http://dx.doi.org/10.1196/annals.1396.043 <jats:p><jats:bold><jats:sc>Abstract</jats:sc>: </jats:bold> <jats:bold>The human immune system evolved to defend the organism against pathogens, but is clearly less well able to do so in the elderly, resulting in greater morbidity and mortality due to infectious disease in old people, and higher healthcare costs. Many age‐associated immune alterations have been reported over the years, of which probably the changes in T cell immunity, often manifested dramatically as large clonal expansions of cells of limited antigen specificity together with a marked shrinkage of the T cell antigen receptor repertoire, are the most notable. It has recently emerged that the common herpesvirus, cytomegalovirus (CMV), which establishes persistent, life‐long infection, usually asymptomatically, may well be the driving force behind clonal expansions and altered phenotypes and functions of CD8 cells seen in most old people. In those few who are not CMV‐infected, another even more common herpesvirus, the Epstein‐Barr virus, appears to have the same effect. These virus‐driven changes are less marked in “successfully aged” centenarians, but most marked in people whom longitudinal studies have shown to be at higher risk of death, that is, those possessing an “immune risk profile” (IRP) characterized by an inverted CD4:8 ratio (caused by the accumulation primarily of CD8<jats:sup>+</jats:sup> CD28<jats:sup>−</jats:sup> cells). These findings support the hypothesis that persistent herpesviruses, especially CMV, act as chronic antigenic stressors and play a major causative role in immunosenescence and associated mortality.</jats:bold> </jats:p> A Driving Force in Human T Cell Immunosenescence Cytomegalovirus Infection : A Driving Force in Human T Cell Immunosenescence Annals of the New York Academy of Sciences |
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10.1196/annals.1396.043 |
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title_sub |
A Driving Force in Human T Cell Immunosenescence |
title |
Cytomegalovirus Infection : A Driving Force in Human T Cell Immunosenescence |
title_unstemmed |
Cytomegalovirus Infection : A Driving Force in Human T Cell Immunosenescence |
title_full |
Cytomegalovirus Infection : A Driving Force in Human T Cell Immunosenescence |
title_fullStr |
Cytomegalovirus Infection : A Driving Force in Human T Cell Immunosenescence |
title_full_unstemmed |
Cytomegalovirus Infection : A Driving Force in Human T Cell Immunosenescence |
title_short |
Cytomegalovirus Infection : A Driving Force in Human T Cell Immunosenescence |
title_sort |
cytomegalovirus infection : a driving force in human t cell immunosenescence |
topic |
History and Philosophy of Science General Biochemistry, Genetics and Molecular Biology General Neuroscience |
url |
http://dx.doi.org/10.1196/annals.1396.043 |
publishDate |
2007 |
physical |
23-35 |
description |
<jats:p><jats:bold><jats:sc>Abstract</jats:sc>: </jats:bold> <jats:bold>The human immune system evolved to defend the organism against pathogens, but is clearly less well able to do so in the elderly, resulting in greater morbidity and mortality due to infectious disease in old people, and higher healthcare costs. Many age‐associated immune alterations have been reported over the years, of which probably the changes in T cell immunity, often manifested dramatically as large clonal expansions of cells of limited antigen specificity together with a marked shrinkage of the T cell antigen receptor repertoire, are the most notable. It has recently emerged that the common herpesvirus, cytomegalovirus (CMV), which establishes persistent, life‐long infection, usually asymptomatically, may well be the driving force behind clonal expansions and altered phenotypes and functions of CD8 cells seen in most old people. In those few who are not CMV‐infected, another even more common herpesvirus, the Epstein‐Barr virus, appears to have the same effect. These virus‐driven changes are less marked in “successfully aged” centenarians, but most marked in people whom longitudinal studies have shown to be at higher risk of death, that is, those possessing an “immune risk profile” (IRP) characterized by an inverted CD4:8 ratio (caused by the accumulation primarily of CD8<jats:sup>+</jats:sup> CD28<jats:sup>−</jats:sup> cells). These findings support the hypothesis that persistent herpesviruses, especially CMV, act as chronic antigenic stressors and play a major causative role in immunosenescence and associated mortality.</jats:bold> </jats:p> |
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author | KOCH, SVEN, LARBI, ANIS, ÖZCELIK, DENNIS, SOLANA, RAFAEL, GOUTTEFANGEAS, CÉCILE, ATTIG, SEBASTIAN, WIKBY, ANDERS, STRINDHALL, JAN, FRANCESCHI, CLAUDIO, PAWELEC, GRAHAM |
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description | <jats:p><jats:bold><jats:sc>Abstract</jats:sc>: </jats:bold> <jats:bold>The human immune system evolved to defend the organism against pathogens, but is clearly less well able to do so in the elderly, resulting in greater morbidity and mortality due to infectious disease in old people, and higher healthcare costs. Many age‐associated immune alterations have been reported over the years, of which probably the changes in T cell immunity, often manifested dramatically as large clonal expansions of cells of limited antigen specificity together with a marked shrinkage of the T cell antigen receptor repertoire, are the most notable. It has recently emerged that the common herpesvirus, cytomegalovirus (CMV), which establishes persistent, life‐long infection, usually asymptomatically, may well be the driving force behind clonal expansions and altered phenotypes and functions of CD8 cells seen in most old people. In those few who are not CMV‐infected, another even more common herpesvirus, the Epstein‐Barr virus, appears to have the same effect. These virus‐driven changes are less marked in “successfully aged” centenarians, but most marked in people whom longitudinal studies have shown to be at higher risk of death, that is, those possessing an “immune risk profile” (IRP) characterized by an inverted CD4:8 ratio (caused by the accumulation primarily of CD8<jats:sup>+</jats:sup> CD28<jats:sup>−</jats:sup> cells). These findings support the hypothesis that persistent herpesviruses, especially CMV, act as chronic antigenic stressors and play a major causative role in immunosenescence and associated mortality.</jats:bold> </jats:p> |
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spelling | KOCH, SVEN LARBI, ANIS ÖZCELIK, DENNIS SOLANA, RAFAEL GOUTTEFANGEAS, CÉCILE ATTIG, SEBASTIAN WIKBY, ANDERS STRINDHALL, JAN FRANCESCHI, CLAUDIO PAWELEC, GRAHAM 0077-8923 1749-6632 Wiley History and Philosophy of Science General Biochemistry, Genetics and Molecular Biology General Neuroscience http://dx.doi.org/10.1196/annals.1396.043 <jats:p><jats:bold><jats:sc>Abstract</jats:sc>: </jats:bold> <jats:bold>The human immune system evolved to defend the organism against pathogens, but is clearly less well able to do so in the elderly, resulting in greater morbidity and mortality due to infectious disease in old people, and higher healthcare costs. Many age‐associated immune alterations have been reported over the years, of which probably the changes in T cell immunity, often manifested dramatically as large clonal expansions of cells of limited antigen specificity together with a marked shrinkage of the T cell antigen receptor repertoire, are the most notable. It has recently emerged that the common herpesvirus, cytomegalovirus (CMV), which establishes persistent, life‐long infection, usually asymptomatically, may well be the driving force behind clonal expansions and altered phenotypes and functions of CD8 cells seen in most old people. In those few who are not CMV‐infected, another even more common herpesvirus, the Epstein‐Barr virus, appears to have the same effect. These virus‐driven changes are less marked in “successfully aged” centenarians, but most marked in people whom longitudinal studies have shown to be at higher risk of death, that is, those possessing an “immune risk profile” (IRP) characterized by an inverted CD4:8 ratio (caused by the accumulation primarily of CD8<jats:sup>+</jats:sup> CD28<jats:sup>−</jats:sup> cells). These findings support the hypothesis that persistent herpesviruses, especially CMV, act as chronic antigenic stressors and play a major causative role in immunosenescence and associated mortality.</jats:bold> </jats:p> A Driving Force in Human T Cell Immunosenescence Cytomegalovirus Infection : A Driving Force in Human T Cell Immunosenescence Annals of the New York Academy of Sciences |
spellingShingle | KOCH, SVEN, LARBI, ANIS, ÖZCELIK, DENNIS, SOLANA, RAFAEL, GOUTTEFANGEAS, CÉCILE, ATTIG, SEBASTIAN, WIKBY, ANDERS, STRINDHALL, JAN, FRANCESCHI, CLAUDIO, PAWELEC, GRAHAM, Annals of the New York Academy of Sciences, Cytomegalovirus Infection : A Driving Force in Human T Cell Immunosenescence, History and Philosophy of Science, General Biochemistry, Genetics and Molecular Biology, General Neuroscience |
title | Cytomegalovirus Infection : A Driving Force in Human T Cell Immunosenescence |
title_full | Cytomegalovirus Infection : A Driving Force in Human T Cell Immunosenescence |
title_fullStr | Cytomegalovirus Infection : A Driving Force in Human T Cell Immunosenescence |
title_full_unstemmed | Cytomegalovirus Infection : A Driving Force in Human T Cell Immunosenescence |
title_short | Cytomegalovirus Infection : A Driving Force in Human T Cell Immunosenescence |
title_sort | cytomegalovirus infection : a driving force in human t cell immunosenescence |
title_sub | A Driving Force in Human T Cell Immunosenescence |
title_unstemmed | Cytomegalovirus Infection : A Driving Force in Human T Cell Immunosenescence |
topic | History and Philosophy of Science, General Biochemistry, Genetics and Molecular Biology, General Neuroscience |
url | http://dx.doi.org/10.1196/annals.1396.043 |