The interplay between immunosenescence and age-related diseases

Abstract

The aging immune system (immunosenescence) has been implicated with increased morbidity and mortality in the elderly. Of note, T cell aging and low-grade inflammation (inflammaging) are implicated with several age-related conditions. The expansion of late-differentiated T cells (CD28 −), regulatory T cells, increased serum levels of autoantibodies, and pro-inflammatory cytokines were implicated with morbidities during aging. Features of accelerated immunosenescence can be identified in adults with chronic inflammatory conditions, such as rheumatoid arthritis, and are predictive of poor clinical outcomes. Therefore, there is an interplay between immunosenescence and age-related diseases. In this review, we discuss how the aging immune system may contribute to the development and clinical course of age-related diseases such as neurodegenerative diseases, rheumatoid arthritis, cancer, cardiovascular, and metabolic diseases.

Cellular senescence: friend or foe to respiratory viral infections?

“…This effect has been partially attributed to defects associated with the ageing of the immune system, termed “immunosenescence”, which is distinct from classical cellular senescence as defined earlier and reviewed elsewhere [ 94 – 96 ]. Briefly, immunosenescence has pleiotropic effects on the immune system including 1) a decrease in the proliferative capacity of haematopoietic stem cells; 2) dysregulation of innate immunity; 3) reduced numbers of naïve T-cells with thymic involution; 4) accumulation of memory T- and B-cells; and 5) a general decline in both T- and B-cell function [ 94 , 97 – 99 ]. Specifically, both CD4 + and CD8 + T-cells from aged hosts ( e.g.…”

The potential of rapalogs to enhance resilience against SARS-CoV-2 infection and reduce the severity of COVID-19

“…Impairment of immune function could also contribute to additional age-associated problems, including in creased prevalence of auto immune disorders and increased risk for numerous types of cancer due to impaired immune surveillance. 9,10 The immune system loses efficacy with age. 9 Immunosenescence affects both innate and acquired immunity and greatly reduces the production of naive T-cells and B-cells in the thymus and bone marrow.…”

The complex relationship between Immunosenescence and Inflammaging: Special issue on the New Biomedical Perspectives

“…This molecular and cellular relationship makes them master regulators and the gear of aging rate. Immunosenescence and inflammaging are key phenomena to understand the onset of ARDs which in turn accelerate the aging process and inflammaging and shortness of life span ( [9,19,20] , FGF21, and humanin and their possible involvement in inflammaging. Although many aspects of mitokine biology are still controversial, the authors discuss the data showing that these mitokines and their immune-metabolic involvement and mechanisms activated by mitochondrial dysfunction have a basic antiinflammatory role and increase with age.…”

“…This molecular and cellular relationship makes them master regulators and the gear of aging rate. Immunosenescence and inflammaging are key phenomena to understand the onset of ARDs which in turn accelerate the aging process and inflammaging and shortness of life span ([ 9 , 19 , 20 ] this issue). Within this scenario, particular attention has been devoted to major ARDs, such as neurodegenerative diseases, rheumatoid arthritis, cancer, and cardiovascular and metabolic diseases [ 19 ].…”

“…Immunosenescence and inflammaging are key phenomena to understand the onset of ARDs which in turn accelerate the aging process and inflammaging and shortness of life span ([ 9 , 19 , 20 ] this issue). Within this scenario, particular attention has been devoted to major ARDs, such as neurodegenerative diseases, rheumatoid arthritis, cancer, and cardiovascular and metabolic diseases [ 19 ]. Along with this interconnection, Xu et al focus on the complex interplay among senescence of immune cells, their different replicative capacity, and cellular turnover, stressing that several types of stimuli and signaling pathways may lead to senescence in the same cell type ([ 20 ] in this issue).…”