Immunosenescence in monocytes, macrophages, and dendritic cells: Lessons learned from the lung and heart

Linton, Phyllis-Jean; Thoman, Marilyn L.

doi:10.1016/j.imlet.2014.06.017

Cited by 68 publications

(52 citation statements)

References 144 publications

(176 reference statements)

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“…Participants in our cohort exhibited similar ranges of immunosenescence marker levels as observed in other recent studies (1–3, 5, 14, 51, 52). In our cohort, females had higher TREC levels and higher CD4/CD8 ratios than the male participants, suggesting that the females in our cohort may be less “immunosenescent” than males, as has been previously observed (53, 54).…”

Section: Discussionsupporting

confidence: 85%

Immunosenescence-Related Transcriptomic and Immunologic Changes in Older Individuals Following Influenza Vaccination

et al. 2016

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The goal of annual influenza vaccination is to reduce mortality and morbidity associated with this disease through the generation of protective immune responses. The objective of the current study was to examine markers of immunosenescence and identify immunosenescence-related differences in gene expression, gene regulation, cytokine secretion, and immunologic changes in an older study population receiving seasonal influenza A/H1N1 vaccination. Surprisingly, prior studies in this cohort revealed weak correlations between immunosenescence markers and humoral immune response to vaccination. In this report, we further examined the relationship of each immunosenescence marker (age, T cell receptor excision circle frequency, telomerase expression, percentage of CD28− CD4+ T cells, percentage of CD28− CD8+ T cells, and the CD4/CD8 T cell ratio) with additional markers of immune response (serum cytokine and chemokine expression) and measures of gene expression and/or regulation. Many of the immunosenescence markers indeed correlated with distinct sets of individual DNA methylation sites, miRNA expression levels, mRNA expression levels, serum cytokines, and leukocyte subsets. However, when the individual immunosenescence markers were grouped by pathways or functional terms, several shared biological functions were identified: antigen processing and presentation pathways, MAPK, mTOR, TCR, BCR, and calcium signaling pathways, as well as key cellular metabolic, proliferation and survival activities. Furthermore, the percent of CD4+ and/or CD8+ T cells lacking CD28 expression also correlated with miRNAs regulating clusters of genes known to be involved in viral infection. Integrated (DNA methylation, mRNA, miRNA, and protein levels) network biology analysis of immunosenescence-related pathways and genesets identified both known pathways (e.g., chemokine signaling, CTL, and NK cell activity), as well as a gene expression module not previously annotated with a known function. These results may improve our ability to predict immune responses to influenza and aid in new vaccine development, and highlight the need for additional studies to better define and characterize immunosenescence.

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Section: Discussionsupporting

confidence: 85%

Immunosenescence-Related Transcriptomic and Immunologic Changes in Older Individuals Following Influenza Vaccination

et al. 2016

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“…ref. ] although they are protagonist immune cells and other experimental methods showed that cardiac macrophages increase during disease .…”

Section: Resultsmentioning

confidence: 99%

Telocytes and putative stem cells in ageing human heart

Popescu

Curici

Wang

et al. 2014

J Cellular Molecular Medi

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Tradition considers that mammalian heart consists of about 70% non-myocytes (interstitial cells) and 30% cardiomyocytes (CMs). Anyway, the presence of telocytes (TCs) has been overlooked, since they were described in 2010 (visit http://www.telocytes.com). Also, the number of cardiac stem cells (CSCs) has not accurately estimated in humans during ageing. We used electron microscopy to identify and estimate the number of cells in human atrial myocardium (appendages). Three age-related groups were studied: newborns (17 days–1 year), children (6–17 years) and adults (34–60 years). Morphometry was performed on low-magnification electron microscope images using computer-assisted technology. We found that interstitial area gradually increases with age from 31.3 ± 4.9% in newborns to 41 ± 5.2% in adults. Also, the number of blood capillaries (per mm2) increased with several hundreds in children and adults versus newborns. CMs are the most numerous cells, representing 76% in newborns, 88% in children and 86% in adults. Images of CMs mitoses were seen in the 17-day newborns. Interestingly, no lipofuscin granules were found in CMs of human newborns and children. The percentage of cells that occupy interstitium were (depending on age): endothelial cells 52–62%; vascular smooth muscle cells and pericytes 22–28%, Schwann cells with nerve endings 6–7%, fibroblasts 3–10%, macrophages 1–8%, TCs about 1% and stem cells less than 1%. We cannot confirm the popular belief that cardiac fibroblasts are the most prevalent cell type in the heart and account for about 20% of myocardial volume. Numerically, TCs represent a small fraction of human cardiac interstitial cells, but because of their extensive telopodes, they achieve a 3D network that, for instance, supports CSCs. The myocardial (very) low capability to regenerate may be explained by the number of CSCs, which decreases fivefold by age (from 0.5% to 0.1% in newborns versus adults).

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“…Monocytes and macrophages cause age‐related deterioration in cytotoxicity, intracellular killing and antigen presentation . Encounter with pathogens results in the activation of macrophages, switching it to a pro‐inflammatory phenotype.…”

Section: Differential Efficiency Of Innate Antiviral Responses In Difmentioning

confidence: 99%

Age has a role in driving host immunopathological response to alphavirus infection

Chan

2017

Immunology

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SummaryAlphaviruses are a group of arthropod-borne pathogens capable of causing a wide spectrum of clinical symptoms, ranging from milder symptoms like rashes, fever and polyarthralgia, to life-threatening encephalitis. This genus of viruses is prevalent globally, and can infect patients across a wide age range. Interestingly, disease severity of virus-infected patients is wideranging. Definitions of the pathogenesis of alphaviruses, as well as the host factors influencing disease severity, remain limited. The innate and adaptive immune systems are important host defences against alphavirus infections. Several reports have highlighted the roles of specific immune subsets in contributing to the immune pathogenesis of these viruses. However, immunosenescence, a gradual deterioration of the immune system brought about by the natural advancement of age, affects the functional roles of these immune subsets. This phenomenon compromises the host's ability to defend against alphavirus infection and pathogenesis. In addition, the lack of maturity in the immune system in newborns and infants also results in more severe disease outcomes. In this review, we will summarize the subtle yet diverse physiological changes in the immune system during aging, and how these changes underlie the differences in disease severity for common alphaviruses.

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Immunosenescence in monocytes, macrophages, and dendritic cells: Lessons learned from the lung and heart

Cited by 68 publications

References 144 publications

Immunosenescence-Related Transcriptomic and Immunologic Changes in Older Individuals Following Influenza Vaccination

Immunosenescence-Related Transcriptomic and Immunologic Changes in Older Individuals Following Influenza Vaccination

Telocytes and putative stem cells in ageing human heart

Age has a role in driving host immunopathological response to alphavirus infection

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