date: 2021-11-22T13:47:26Z
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pdf:docinfo:title: How Immunosenescence and Inflammaging May Contribute to Hyperinflammatory Syndrome in COVID-19
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subject: 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.
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dc:title: How Immunosenescence and Inflammaging May Contribute to Hyperinflammatory Syndrome in COVID-19
modified: 2021-11-22T13:47:26Z
cp:subject: 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.
pdf:docinfo:subject: 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.
pdf:docinfo:creator: Ludmila Müller and Svetlana Di Benedetto
meta:author: Ludmila Müller and Svetlana Di Benedetto
meta:creation-date: 2021-11-21T09:07:49Z
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Creation-Date: 2021-11-21T09:07:49Z
Author: Ludmila Müller and Svetlana Di Benedetto
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dc: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.
Keywords: aging; immunosenescence; inflammaging; cytokine storm; senescence-associated secretory phenotype (SASP); CMV; hyperinflammatory syndrome; COVID-19
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dc:creator: Ludmila Müller and Svetlana Di Benedetto
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.
dcterms:created: 2021-11-21T09:07:49Z
Last-Modified: 2021-11-22T13:47:26Z
dcterms:modified: 2021-11-22T13:47:26Z
title: How Immunosenescence and Inflammaging May Contribute to Hyperinflammatory Syndrome in COVID-19
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pdf:docinfo:keywords: aging; immunosenescence; inflammaging; cytokine storm; senescence-associated secretory phenotype (SASP); CMV; hyperinflammatory syndrome; COVID-19
pdf:docinfo:modified: 2021-11-22T13:47:26Z
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creator: Ludmila Müller and Svetlana Di Benedetto
dc:subject: aging; immunosenescence; inflammaging; cytokine storm; senescence-associated secretory phenotype (SASP); CMV; hyperinflammatory syndrome; COVID-19
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meta:keyword: aging; immunosenescence; inflammaging; cytokine storm; senescence-associated secretory phenotype (SASP); CMV; hyperinflammatory syndrome; COVID-19
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pdf:docinfo:created: 2021-11-21T09:07:49Z