Effects of Immunosenescence on the Lower Expression of Surface Molecules in Neutrophils and Lymphocytes

Lopes, Alessandra Barbosa; Lopes, Larissa Barbosa; Antunes, Roseli Nunes da Silveira; Fukasawa, Josianne Thomazini; Cavaretto, Debora de Aguiar; Calamita, Zamir

doi:10.2174/1874609811666180605092234

Cited by 10 publications

(7 citation statements)

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“…However, an excessive accumulation of neutrophils and hyper-responsiveness can be detrimental and cause tissue injury, as recently documented in subjects with lethal COVID-19 ( 159 , 160 ). Although no difference has been found in the number of neutrophils between young and older adults, aged neutrophils exhibit a dysfunctional phagocytic and chemotactic capacity ( 28 , 161 , 162 ). In aged mice, these dysfunctional cells expand and accumulate in lymph nodes due to impaired apoptosis ( 163 , 164 ).…”

Section: Age-associated Immune Cell Dysfunctionsmentioning

confidence: 97%

Aging and Options to Halt Declining Immunity to Virus Infections

et al. 2021

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Immunosenescence is a process associated with aging that leads to dysregulation of cells of innate and adaptive immunity, which may become dysfunctional. Consequently, older adults show increased severity of viral and bacterial infections and impaired responses to vaccinations. A better understanding of the process of immunosenescence will aid the development of novel strategies to boost the immune system in older adults. In this review, we focus on major alterations of the immune system triggered by aging, and address the effect of chronic viral infections, effectiveness of vaccination of older adults and strategies to improve immune function in this vulnerable age group.

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Section: Age-associated Immune Cell Dysfunctionsmentioning

confidence: 97%

Aging and Options to Halt Declining Immunity to Virus Infections

et al. 2021

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“…However, aging appears to promote a dysfunctional chemotactic capacity in neutrophils, which alters both dissemination and achievement of the site of damage. This is demonstrated by phenotypic changes, such as: (i) decreased expression of CD11b, which is involved in the recruitment of neutrophils to the infected tissue; (ii) up-regulation of chemokine receptors and adhesion molecules CXCR4, CD49d, and ICAM, which facilitate neutrophil migration through the endothelium; (iii) down-regulation of chemokine receptor CXCR2 which determines the capacity to reverse-transmigrate in the vessels; (iv) decreased mobilisation of actin and calcium related to the migration capacity [ 21 , 22 , 23 ]. Defects in chemotaxis and, consequently, in the ability to reach the site of damage, lead to altered neutrophil distribution, which also impairs pathogen recognition and elimination.…”

Section: Immunosenescence Of the Innate Immune Cellsmentioning

confidence: 99%

How Can We Improve Vaccination Response in Old People? Part I: Targeting Immunosenescence of Innate Immunity Cells

Aiello

Ligotti

Garnica

et al. 2022

IJMS

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Vaccination, being able to prevent millions of cases of infectious diseases around the world every year, is the most effective medical intervention ever introduced. However, immunosenescence makes vaccines less effective in providing protection to older people. Although most studies explain that this is mainly due to the immunosenescence of T and B cells, the immunosenescence of innate immunity can also be a significant contributing factor. Alterations in function, number, subset, and distribution of blood neutrophils, monocytes, and natural killer and dendritic cells are detected in aging, thus potentially reducing the efficacy of vaccines in older individuals. In this paper, we focus on the immunosenescence of the innate blood immune cells. We discuss possible strategies to counteract the immunosenescence of innate immunity in order to improve the response to vaccination. In particular, we focus on advances in understanding the role and the development of new adjuvants, such as TLR agonists, considered a promising strategy to increase vaccination efficiency in older individuals.

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“…However, there was still significant difference between KT high-dose group and the young control group. It is supposed that thymus atrophied with the prolonging of the experiment which led to the number of lymphocytes decline and function degraded (Lopes et al, 2018, Zhou et al, 2018.…”

Section: G0/g1 + S + G2mmentioning

confidence: 99%

Influences of 6-furfuryloaminopurine on Peripheral T Lymphocyte Subpopulations and Apoptosis of Thymus Lymphocytes of Aging Rats

Li¹,

liu²,

Fu³

et al. 2021

IJAR

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Background: 6-furfuryloaminopurine (KT) is the first compound to be identified as a cytokinin. Despite that there are many studies related to KT but the mechanism of KT in resisting immunosenescence remains unclear. The objective of this study is to investigate the influences of KT on the immunity of thymus in rats by detecting the apoptosis and the proliferation index (PI).Methods: We firstly established an aging rat model by subcutaneously injecting D- galactose (D-gal, 125mg/kg•BW) in the dorsal neck of Sprague Daly rats (SD rats); then the rats were divided into KT treatment groups (three groups for different doses of KT), aging model group (without KT treatment) and young control group. The rats in KT treatment groups were treated with different-dose KT and the key indices including the changes of the number of CD3+, CD4+ and CD8+ T lymphocyte subpopulations in peripheral blood, the apoptosis of thymus lymphocytes. Result: KT could increase the number of the peripheral CD3+, CD4+ and CD8+ T lymphocytes of the aging rats while decreased the apoptotic rate of thymocytes and increased PI Index.

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Effects of Immunosenescence on the Lower Expression of Surface Molecules in Neutrophils and Lymphocytes

Cited by 10 publications

References 0 publications

Aging and Options to Halt Declining Immunity to Virus Infections

Aging and Options to Halt Declining Immunity to Virus Infections

How Can We Improve Vaccination Response in Old People? Part I: Targeting Immunosenescence of Innate Immunity Cells

Influences of 6-furfuryloaminopurine on Peripheral T Lymphocyte Subpopulations and Apoptosis of Thymus Lymphocytes of Aging Rats

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