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Is inflammaging an auto[innate]immunity subclinical syndrome?
The low-grade, chronic, systemic inflammatory state that characterizes the aging process (inflammaging) results from late evolutive-based expression of the innate immune system. Inflammaging is characterized by the complex set of five conditions which can be described as 1. low-grade, 2. controlled,...
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2006
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1716179/ https://www.ncbi.nlm.nih.gov/pubmed/17173699 http://dx.doi.org/10.1186/1742-4933-3-12 |
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author | Giunta, Sergio |
author_facet | Giunta, Sergio |
author_sort | Giunta, Sergio |
collection | PubMed |
description | The low-grade, chronic, systemic inflammatory state that characterizes the aging process (inflammaging) results from late evolutive-based expression of the innate immune system. Inflammaging is characterized by the complex set of five conditions which can be described as 1. low-grade, 2. controlled, 3. asymptomatic, 4. chronic, 5. systemic, inflammatory state, and fits with the antagonistic pleiotropy theory on the evolution of aging postulating that senescence is the late deleterious effect of genes (pro-inflammatory versus anti-inflammatory)that are beneficial in early life. Evolutionary programming of the innate immune system may act via selection on these genetic traits. Here I propose that the already acquired knowledge in this field may pave the way to a new chapter in the pathophysiology of autoimmunity: the auto-innate-immunity syndromes. Indeed, differently from the well known chapter of conventional autoimmune diseases and syndromes where the main actor is the adaptive immunity, inflammaging may constitute the subclinical paradigm of a new chapter of autoimmunity, namely that arising from an autoimmune inflammatory response of the innate-immune-system, an old actor of immunity and yet a new actor of autoimmunity, also acting as a major determinant of elderly frailty and age-associated diseases. |
format | Text |
id | pubmed-1716179 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2006 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-17161792006-12-22 Is inflammaging an auto[innate]immunity subclinical syndrome? Giunta, Sergio Immun Ageing Hypothesis The low-grade, chronic, systemic inflammatory state that characterizes the aging process (inflammaging) results from late evolutive-based expression of the innate immune system. Inflammaging is characterized by the complex set of five conditions which can be described as 1. low-grade, 2. controlled, 3. asymptomatic, 4. chronic, 5. systemic, inflammatory state, and fits with the antagonistic pleiotropy theory on the evolution of aging postulating that senescence is the late deleterious effect of genes (pro-inflammatory versus anti-inflammatory)that are beneficial in early life. Evolutionary programming of the innate immune system may act via selection on these genetic traits. Here I propose that the already acquired knowledge in this field may pave the way to a new chapter in the pathophysiology of autoimmunity: the auto-innate-immunity syndromes. Indeed, differently from the well known chapter of conventional autoimmune diseases and syndromes where the main actor is the adaptive immunity, inflammaging may constitute the subclinical paradigm of a new chapter of autoimmunity, namely that arising from an autoimmune inflammatory response of the innate-immune-system, an old actor of immunity and yet a new actor of autoimmunity, also acting as a major determinant of elderly frailty and age-associated diseases. BioMed Central 2006-12-16 /pmc/articles/PMC1716179/ /pubmed/17173699 http://dx.doi.org/10.1186/1742-4933-3-12 Text en Copyright © 2006 Giunta; 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 | Hypothesis Giunta, Sergio Is inflammaging an auto[innate]immunity subclinical syndrome? |
title | Is inflammaging an auto[innate]immunity subclinical syndrome? |
title_full | Is inflammaging an auto[innate]immunity subclinical syndrome? |
title_fullStr | Is inflammaging an auto[innate]immunity subclinical syndrome? |
title_full_unstemmed | Is inflammaging an auto[innate]immunity subclinical syndrome? |
title_short | Is inflammaging an auto[innate]immunity subclinical syndrome? |
title_sort | is inflammaging an auto[innate]immunity subclinical syndrome? |
topic | Hypothesis |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1716179/ https://www.ncbi.nlm.nih.gov/pubmed/17173699 http://dx.doi.org/10.1186/1742-4933-3-12 |
work_keys_str_mv | AT giuntasergio isinflammaginganautoinnateimmunitysubclinicalsyndrome |