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Immune Deficiencies at the Extremes of Age

In early life as well as in late life, the immune system is dysfunctional. During early infancy, innate as well as adaptive immune cells are immature, immune memory has not been built, and regulatory pathways that maintain tolerance dominate. Throughout life, the adult human systems face the challen...

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Detalles Bibliográficos
Autores principales: Goronzy, Jӧrg J., Gustafson, Claire E., Weyand, Cornelia M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7150132/
http://dx.doi.org/10.1016/B978-0-7020-6896-6.00038-7
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author Goronzy, Jӧrg J.
Gustafson, Claire E.
Weyand, Cornelia M.
author_facet Goronzy, Jӧrg J.
Gustafson, Claire E.
Weyand, Cornelia M.
author_sort Goronzy, Jӧrg J.
collection PubMed
description In early life as well as in late life, the immune system is dysfunctional. During early infancy, innate as well as adaptive immune cells are immature, immune memory has not been built, and regulatory pathways that maintain tolerance dominate. Throughout life, the adult human systems face the challenge of maintaining immune cell and population homeostasis while facing declining regenerative capacity and constant exogenous assaults. Failure of homeostatic mechanisms, together with age-acquired cellular defects, leads to the complex embodiment of immunosenescence that combines ineffective immune responses to infection and vaccination with constitutive production of inflammatory mediators and increased risk of autoimmunity.
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spelling pubmed-71501322020-04-13 Immune Deficiencies at the Extremes of Age Goronzy, Jӧrg J. Gustafson, Claire E. Weyand, Cornelia M. Clinical Immunology Article In early life as well as in late life, the immune system is dysfunctional. During early infancy, innate as well as adaptive immune cells are immature, immune memory has not been built, and regulatory pathways that maintain tolerance dominate. Throughout life, the adult human systems face the challenge of maintaining immune cell and population homeostasis while facing declining regenerative capacity and constant exogenous assaults. Failure of homeostatic mechanisms, together with age-acquired cellular defects, leads to the complex embodiment of immunosenescence that combines ineffective immune responses to infection and vaccination with constitutive production of inflammatory mediators and increased risk of autoimmunity. 2019 2018-03-13 /pmc/articles/PMC7150132/ http://dx.doi.org/10.1016/B978-0-7020-6896-6.00038-7 Text en Copyright © 2019 Elsevier Ltd. All rights reserved. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.
spellingShingle Article
Goronzy, Jӧrg J.
Gustafson, Claire E.
Weyand, Cornelia M.
Immune Deficiencies at the Extremes of Age
title Immune Deficiencies at the Extremes of Age
title_full Immune Deficiencies at the Extremes of Age
title_fullStr Immune Deficiencies at the Extremes of Age
title_full_unstemmed Immune Deficiencies at the Extremes of Age
title_short Immune Deficiencies at the Extremes of Age
title_sort immune deficiencies at the extremes of age
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7150132/
http://dx.doi.org/10.1016/B978-0-7020-6896-6.00038-7
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