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Age-related autoimmunity

Older persons have higher autoimmunity but a lower prevalence of autoimmune diseases. A possible explanation for this is the expansion of many protective regulatory mechanisms highly characteristic in the elderly. Of note is the higher production of peripheral T-regulatory cells. The frequent develo...

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Autores principales: Vadasz, Zahava, Haj, Tharwat, Kessel, Aharon, Toubi, Elias
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3616810/
https://www.ncbi.nlm.nih.gov/pubmed/23556986
http://dx.doi.org/10.1186/1741-7015-11-94
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author Vadasz, Zahava
Haj, Tharwat
Kessel, Aharon
Toubi, Elias
author_facet Vadasz, Zahava
Haj, Tharwat
Kessel, Aharon
Toubi, Elias
author_sort Vadasz, Zahava
collection PubMed
description Older persons have higher autoimmunity but a lower prevalence of autoimmune diseases. A possible explanation for this is the expansion of many protective regulatory mechanisms highly characteristic in the elderly. Of note is the higher production of peripheral T-regulatory cells. The frequent development of autoimmunity in the elderly was suggested to take place in part due to the selection of T cells with increased affinity to self-antigens or to latent viruses. These cells were shown to have a greater ability to be pro-inflammatory, thereby amplifying autoimmunity. During aging, thymic T-regulatory cell output decreases in association with the loss of thymic capacity to generate new T cells. However, to balance the above mentioned autoimmunity and prevent the development of autoimmune diseases, there is an age-related increase in peripheral CD4+ CD25highFoxP3+ T-regulatory cells. It remains unclear whether this is an age-related immune dysfunction or a defense response. Whatever the reason, the expansion of T-regulatory cells requires payment in terms of an increased incidence of cancer and higher susceptibility to infections.
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spelling pubmed-36168102013-04-05 Age-related autoimmunity Vadasz, Zahava Haj, Tharwat Kessel, Aharon Toubi, Elias BMC Med Commentary Older persons have higher autoimmunity but a lower prevalence of autoimmune diseases. A possible explanation for this is the expansion of many protective regulatory mechanisms highly characteristic in the elderly. Of note is the higher production of peripheral T-regulatory cells. The frequent development of autoimmunity in the elderly was suggested to take place in part due to the selection of T cells with increased affinity to self-antigens or to latent viruses. These cells were shown to have a greater ability to be pro-inflammatory, thereby amplifying autoimmunity. During aging, thymic T-regulatory cell output decreases in association with the loss of thymic capacity to generate new T cells. However, to balance the above mentioned autoimmunity and prevent the development of autoimmune diseases, there is an age-related increase in peripheral CD4+ CD25highFoxP3+ T-regulatory cells. It remains unclear whether this is an age-related immune dysfunction or a defense response. Whatever the reason, the expansion of T-regulatory cells requires payment in terms of an increased incidence of cancer and higher susceptibility to infections. BioMed Central 2013-04-04 /pmc/articles/PMC3616810/ /pubmed/23556986 http://dx.doi.org/10.1186/1741-7015-11-94 Text en Copyright © 2013 Vadasz et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Commentary
Vadasz, Zahava
Haj, Tharwat
Kessel, Aharon
Toubi, Elias
Age-related autoimmunity
title Age-related autoimmunity
title_full Age-related autoimmunity
title_fullStr Age-related autoimmunity
title_full_unstemmed Age-related autoimmunity
title_short Age-related autoimmunity
title_sort age-related autoimmunity
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3616810/
https://www.ncbi.nlm.nih.gov/pubmed/23556986
http://dx.doi.org/10.1186/1741-7015-11-94
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