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Autologous NK cells propagated and activated ex vivo decrease senescence markers in human PBMCs
Aging is a multifactorial process involving many steps including senescence. The immune system plays a critical role in aging where chronic inflammation and senescence has been shown to be detrimental. Natural killer (NK) cells are the predominant innate lymphocyte subset that mediate various respon...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9661662/ https://www.ncbi.nlm.nih.gov/pubmed/36386442 http://dx.doi.org/10.1016/j.bbrep.2022.101380 |
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author | Chelyapov, Nickolas Nguyen, Toai T Gonzalez, Rafael |
author_facet | Chelyapov, Nickolas Nguyen, Toai T Gonzalez, Rafael |
author_sort | Chelyapov, Nickolas |
collection | PubMed |
description | Aging is a multifactorial process involving many steps including senescence. The immune system plays a critical role in aging where chronic inflammation and senescence has been shown to be detrimental. Natural killer (NK) cells are the predominant innate lymphocyte subset that mediate various responses to include surveillance and elimination of senescent cells. Here, we use autologous propagated and activated NK (aNK) cells from 5 patients to demonstrate that aNK cells decrease senescent cells in vitro and immunosenescence in humans based on markers p16 and β-galactosidase. In addition, inflammatory cytokine panel data suggest a role for removal of immunosenescence to reduce the aging-related inflammatory response. |
format | Online Article Text |
id | pubmed-9661662 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-96616622022-11-15 Autologous NK cells propagated and activated ex vivo decrease senescence markers in human PBMCs Chelyapov, Nickolas Nguyen, Toai T Gonzalez, Rafael Biochem Biophys Rep Short Communication Aging is a multifactorial process involving many steps including senescence. The immune system plays a critical role in aging where chronic inflammation and senescence has been shown to be detrimental. Natural killer (NK) cells are the predominant innate lymphocyte subset that mediate various responses to include surveillance and elimination of senescent cells. Here, we use autologous propagated and activated NK (aNK) cells from 5 patients to demonstrate that aNK cells decrease senescent cells in vitro and immunosenescence in humans based on markers p16 and β-galactosidase. In addition, inflammatory cytokine panel data suggest a role for removal of immunosenescence to reduce the aging-related inflammatory response. Elsevier 2022-11-11 /pmc/articles/PMC9661662/ /pubmed/36386442 http://dx.doi.org/10.1016/j.bbrep.2022.101380 Text en © 2022 The Authors. Published by Elsevier B.V. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Short Communication Chelyapov, Nickolas Nguyen, Toai T Gonzalez, Rafael Autologous NK cells propagated and activated ex vivo decrease senescence markers in human PBMCs |
title | Autologous NK cells propagated and activated ex vivo decrease senescence markers in human PBMCs |
title_full | Autologous NK cells propagated and activated ex vivo decrease senescence markers in human PBMCs |
title_fullStr | Autologous NK cells propagated and activated ex vivo decrease senescence markers in human PBMCs |
title_full_unstemmed | Autologous NK cells propagated and activated ex vivo decrease senescence markers in human PBMCs |
title_short | Autologous NK cells propagated and activated ex vivo decrease senescence markers in human PBMCs |
title_sort | autologous nk cells propagated and activated ex vivo decrease senescence markers in human pbmcs |
topic | Short Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9661662/ https://www.ncbi.nlm.nih.gov/pubmed/36386442 http://dx.doi.org/10.1016/j.bbrep.2022.101380 |
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