The role of the T cell in age-related inflammation.
Identifieur interne : 000586 ( PubMed/Corpus ); précédent : 000585; suivant : 000587The role of the T cell in age-related inflammation.
Auteurs : Richard Macaulay ; Arne N. Akbar ; Sian M. HensonSource :
- Age (Dordrecht, Netherlands) [ 1574-4647 ] ; 2013.
English descriptors
- KwdEn :
- MESH :
- chemical , immunology : Cytokines.
- immunology : Aging, Inflammation, T-Lymphocytes.
- chemical , metabolism : Cytokines, T-Lymphocytes.
- pathology : Aging, Inflammation, T-Lymphocytes.
- physiology : Longevity.
- Animals, Humans.
Abstract
Ageing is accompanied by alterations to T-cell immunity and also by a low-grade chronic inflammatory state termed inflammaging. The significance of these phenomena is highlighted by their being predictors of earlier mortality. We have recently published that the proinflammatory cytokine TNFα is a strong inducer of CD4(+) T-cell senescence and T-cell differentiation, adding to the growing body of literature implicating proinflammatory molecules in mediating these critical age-related T-cell alterations. Moreover, the inflammatory process is also being increasingly implicated in the pathogenesis of many common and severe age-related diseases, including cancer, cardiovascular diseases and type 2 diabetes. Furthermore, major age-related risk factors for poor health, such as obesity, stress and smoking, are also associated with an upregulation in systemic inflammatory markers. We propose the idea that the ensuing inflammatory response to influenza infection propagates cardiovascular diseases and constitutes a major cause of influenza-related mortality. While inflammation is not a negative phenomenon per se, this age-related dysregulation of inflammatory responses may play crucial roles driving age-related pathologies, T-cell immunosenescence and CMV reactivation, thereby underpinning key features of the ageing process.
DOI: 10.1007/s11357-012-9381-2
PubMed: 22252437
Links to Exploration step
pubmed:22252437Le document en format XML
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Henson</name></author></analytic><series><title level="j">Age (Dordrecht, Netherlands)</title><idno type="eISSN">1574-4647</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aging (immunology)</term><term>Aging (pathology)</term><term>Animals</term><term>Cytokines (immunology)</term><term>Cytokines (metabolism)</term><term>Humans</term><term>Inflammation (immunology)</term><term>Inflammation (pathology)</term><term>Longevity (physiology)</term><term>T-Lymphocytes (immunology)</term><term>T-Lymphocytes (metabolism)</term><term>T-Lymphocytes (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Aging</term><term>Inflammation</term><term>T-Lymphocytes</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term><term>T-Lymphocytes</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Aging</term><term>Inflammation</term><term>T-Lymphocytes</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Longevity</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Ageing is accompanied by alterations to T-cell immunity and also by a low-grade chronic inflammatory state termed inflammaging. The significance of these phenomena is highlighted by their being predictors of earlier mortality. We have recently published that the proinflammatory cytokine TNFα is a strong inducer of CD4(+) T-cell senescence and T-cell differentiation, adding to the growing body of literature implicating proinflammatory molecules in mediating these critical age-related T-cell alterations. Moreover, the inflammatory process is also being increasingly implicated in the pathogenesis of many common and severe age-related diseases, including cancer, cardiovascular diseases and type 2 diabetes. Furthermore, major age-related risk factors for poor health, such as obesity, stress and smoking, are also associated with an upregulation in systemic inflammatory markers. We propose the idea that the ensuing inflammatory response to influenza infection propagates cardiovascular diseases and constitutes a major cause of influenza-related mortality. While inflammation is not a negative phenomenon per se, this age-related dysregulation of inflammatory responses may play crucial roles driving age-related pathologies, T-cell immunosenescence and CMV reactivation, thereby underpinning key features of the ageing process.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22252437</PMID><DateCompleted><Year>2013</Year><Month>10</Month><Day>17</Day></DateCompleted><DateRevised><Year>2019</Year><Month>10</Month><Day>08</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1574-4647</ISSN><JournalIssue CitedMedium="Internet"><Volume>35</Volume><Issue>3</Issue><PubDate><Year>2013</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Age (Dordrecht, Netherlands)</Title><ISOAbbreviation>Age (Dordr)</ISOAbbreviation></Journal><ArticleTitle>The role of the T cell in age-related inflammation.</ArticleTitle><Pagination><MedlinePgn>563-72</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s11357-012-9381-2</ELocationID><Abstract><AbstractText>Ageing is accompanied by alterations to T-cell immunity and also by a low-grade chronic inflammatory state termed inflammaging. The significance of these phenomena is highlighted by their being predictors of earlier mortality. We have recently published that the proinflammatory cytokine TNFα is a strong inducer of CD4(+) T-cell senescence and T-cell differentiation, adding to the growing body of literature implicating proinflammatory molecules in mediating these critical age-related T-cell alterations. Moreover, the inflammatory process is also being increasingly implicated in the pathogenesis of many common and severe age-related diseases, including cancer, cardiovascular diseases and type 2 diabetes. Furthermore, major age-related risk factors for poor health, such as obesity, stress and smoking, are also associated with an upregulation in systemic inflammatory markers. We propose the idea that the ensuing inflammatory response to influenza infection propagates cardiovascular diseases and constitutes a major cause of influenza-related mortality. While inflammation is not a negative phenomenon per se, this age-related dysregulation of inflammatory responses may play crucial roles driving age-related pathologies, T-cell immunosenescence and CMV reactivation, thereby underpinning key features of the ageing process.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Macaulay</LastName><ForeName>Richard</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Division of Infection and Immunity, Rayne Institute, University College London, 5 University Street, London, WC1E 6JF, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Akbar</LastName><ForeName>Arne N</ForeName><Initials>AN</Initials></Author><Author ValidYN="Y"><LastName>Henson</LastName><ForeName>Sian M</ForeName><Initials>SM</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>BB/J006750/1</GrantID><Agency>Biotechnology and Biological Sciences Research 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