How Immunosenescence and Inflammaging May Contribute to Hyperinflammatory Syndrome in COVID-19

Aging is characterized by the dynamic remodeling of the immune system designated “immunosenescence,” and is associated with altered hematopoiesis, thymic involution, and lifelong immune stimulation by multitudinous chronic stressors, including the cytomegalovirus (CMV). Such alterations may contribu...

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Autores principales:	Ludmila Müller, Svetlana Di Benedetto
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	aging immunosenescence inflammaging cytokine storm senescence-associated secretory phenotype (SASP) CMV Biology (General) QH301-705.5 Chemistry QD1-999
Acceso en línea:	https://doaj.org/article/e1fbb81fea374715ae2608ec150e55f3
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spelling	oai:doaj.org-article:e1fbb81fea374715ae2608ec150e55f32021-11-25T17:57:37ZHow Immunosenescence and Inflammaging May Contribute to Hyperinflammatory Syndrome in COVID-1910.3390/ijms2222125391422-00671661-6596https://doaj.org/article/e1fbb81fea374715ae2608ec150e55f32021-11-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/22/12539https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067Aging is characterized by the dynamic remodeling of the immune system designated “immunosenescence,” and is associated with altered hematopoiesis, thymic involution, and lifelong immune stimulation by multitudinous chronic stressors, including the cytomegalovirus (CMV). Such alterations may contribute to a lowered proportion of naïve T-cells and to reduced diversity of the T-cell repertoire. In the peripheral circulation, a shift occurs towards accumulations of T and B-cell populations with memory phenotypes, and to accumulation of putatively senescent and exhausted immune cells. The aging-related accumulations of functionally exhausted memory T lymphocytes, commonly secreting pro-inflammatory cytokines, together with mediators and factors of the innate immune system, are considered to contribute to the low-grade inflammation (inflammaging) often observed in elderly people. These senescent immune cells not only secrete inflammatory mediators, but are also able to negatively modulate their environments. In this review, we give a short summary of the ways that immunosenescence, inflammaging, and CMV infection may cause insufficient immune responses, contribute to the establishment of the hyperinflammatory syndrome and impact the severity of the coronavirus disease 2019 (COVID-19) in elderly people.Ludmila MüllerSvetlana Di BenedettoMDPI AGarticleagingimmunosenescenceinflammagingcytokine stormsenescence-associated secretory phenotype (SASP)CMVBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 12539, p 12539 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	aging immunosenescence inflammaging cytokine storm senescence-associated secretory phenotype (SASP) CMV Biology (General) QH301-705.5 Chemistry QD1-999
spellingShingle	aging immunosenescence inflammaging cytokine storm senescence-associated secretory phenotype (SASP) CMV Biology (General) QH301-705.5 Chemistry QD1-999 Ludmila Müller Svetlana Di Benedetto How Immunosenescence and Inflammaging May Contribute to Hyperinflammatory Syndrome in COVID-19
description	Aging is characterized by the dynamic remodeling of the immune system designated “immunosenescence,” and is associated with altered hematopoiesis, thymic involution, and lifelong immune stimulation by multitudinous chronic stressors, including the cytomegalovirus (CMV). Such alterations may contribute to a lowered proportion of naïve T-cells and to reduced diversity of the T-cell repertoire. In the peripheral circulation, a shift occurs towards accumulations of T and B-cell populations with memory phenotypes, and to accumulation of putatively senescent and exhausted immune cells. The aging-related accumulations of functionally exhausted memory T lymphocytes, commonly secreting pro-inflammatory cytokines, together with mediators and factors of the innate immune system, are considered to contribute to the low-grade inflammation (inflammaging) often observed in elderly people. These senescent immune cells not only secrete inflammatory mediators, but are also able to negatively modulate their environments. In this review, we give a short summary of the ways that immunosenescence, inflammaging, and CMV infection may cause insufficient immune responses, contribute to the establishment of the hyperinflammatory syndrome and impact the severity of the coronavirus disease 2019 (COVID-19) in elderly people.
format	article
author	Ludmila Müller Svetlana Di Benedetto
author_facet	Ludmila Müller Svetlana Di Benedetto
author_sort	Ludmila Müller
title	How Immunosenescence and Inflammaging May Contribute to Hyperinflammatory Syndrome in COVID-19
title_short	How Immunosenescence and Inflammaging May Contribute to Hyperinflammatory Syndrome in COVID-19
title_full	How Immunosenescence and Inflammaging May Contribute to Hyperinflammatory Syndrome in COVID-19
title_fullStr	How Immunosenescence and Inflammaging May Contribute to Hyperinflammatory Syndrome in COVID-19
title_full_unstemmed	How Immunosenescence and Inflammaging May Contribute to Hyperinflammatory Syndrome in COVID-19
title_sort	how immunosenescence and inflammaging may contribute to hyperinflammatory syndrome in covid-19
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/e1fbb81fea374715ae2608ec150e55f3
work_keys_str_mv	AT ludmilamuller howimmunosenescenceandinflammagingmaycontributetohyperinflammatorysyndromeincovid19 AT svetlanadibenedetto howimmunosenescenceandinflammagingmaycontributetohyperinflammatorysyndromeincovid19
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How Immunosenescence and Inflammaging May Contribute to Hyperinflammatory Syndrome in COVID-19

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