Decreased absolute numbers of CD3+ T cells and CD8+ T cells during aging in herpes zoster patients

Li, Wei; Zhao, Jianguang; Wu, Wei; Fu, Xin; Chen, Lifeng; Wang, Xiaoting

doi:10.1038/s41598-017-15390-w

Cited by 34 publications

(35 citation statements)

References 35 publications

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“…The analysis of the number and percentage of CD3+ and CD3+CD56+ lymphocytes performed in our study corresponded to the investigations of the other groups and showed the increase in the number of NKT-like cells in the process of ageing [4,6,48] and decrease in the number and percentage of T lymphocytes [48][49][50].…”

Section: Nkt-like Cells Are "Non-classical" Nkt Cells Which Representsupporting

confidence: 84%

NKT-like cells reveal higher than T lymphocytes expression of cellular protective proteins HSP70 and SOD2 and comparably increased expression of SIRT1 in the oldest seniors

Kaszubowska

Foerster

Kwiatkowski

et al. 2019

Folia Histochem Cytobiol.

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Introduction. NKT-like cells are "non-classical", "CD1d-independent" NKT cells which represent highly differentiated, conventional T lymphocytes coexpressing several NK (natural killer) associated receptors. They are effector lymphocytes of both innate and adaptive immunity and simultaneously regulatory cells of the adaptive immune system. They reveal large granular lymphocyte morphology and can mediate both MHC-restricted and MHC-unrestricted cytotoxicity, secrete many cytokines and modulate Th1 immune responses. The aim of our study was to analyze the expression of proteins involved in cellular stress response: sirtuin 1 (SIRT1), heat shock protein 70 (HSP70) and manganese superoxide dismutase (SOD2) in NKT-like cells compared to T lymphocytes during ageing. Material and methods. The study involved three groups of participants: the oldest seniors (n = 25; aged over 85; mean age 88 ± 0.5 ys), the old (n = 30; aged under 85; mean age 76 ± 0.9 ys) and the young (n = 32; mean age 21 ± 0.3 ys). Whole blood samples were analyzed by flow cytometry to assess NKT-like (CD3+CD56+) and T (CD3+) cell populations. Results. The group of the oldest seniors differed from the other age groups by much higher percentage of both NKT-like cells and T lymphocytes expressing SIRT1, HSP70 and SOD2. The expression of these proteins correlated positively with the age of the participants. Interestingly, the significantly higher expression of the studied protective proteins; i.e. HSP70 and SOD2 was found in CD3+CD56+ cells compared to CD3+ lymphocytes and this phenomenon concerned all the studied age groups. These differences were not significant regarding the expression of SIRT1; however, the same tendency was noticeable. Conclusions. The analysis of CD3+ and CD3+CD56+ lymphocytes showed the increase in the number of NKT-like cells and decreased number of T cells in the process of ageing. The increased expression of cellular protective proteins SIRT1, HSP70 and SOD2 in NKT-like and T-lymphocytes of the oldest seniors seems to correspond to longevity and the observed correlations may suggest the involvement of these proteins in establishing cellular homeostasis specific for healthy ageing. Furthermore, the higher expression of the protective proteins in NKT-like cells compared to T lymphocytes may indicate their particular role in the interplay between innate and adaptive immunity responses during the process of ageing.

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Section: Nkt-like Cells Are "Non-classical" Nkt Cells Which Representsupporting

confidence: 84%

NKT-like cells reveal higher than T lymphocytes expression of cellular protective proteins HSP70 and SOD2 and comparably increased expression of SIRT1 in the oldest seniors

Kaszubowska

Foerster

Kwiatkowski

et al. 2019

Folia Histochem Cytobiol.

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“…Although we saw no changes in total T cell or CD8 + numbers, our mice are only aged to 14-16 months which is more like middle-aged humans (40-60 years) than truly elderly patients [41]. Human data suggests that the total number of T cells, and specifically CD8+ T cells, doesn't change between young (<40 years) and middle-aged (40-60 years) groups, however it significantly decreases in the old (>60 years) age group [42]. Perhaps if mice were aged >18-months we may see a T cell dependent effect.…”

Section: Discussionmentioning

confidence: 85%

Platelet-derived β2m regulates age related monocyte/macrophage functions

Hilt

Ture

Mohan

et al. 2019

Aging

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Platelets have central roles in both immune responses and development. Stimulated platelets express leukocyte adhesion molecules and release numerous immune modulatory factors that recruit and activate leukocytes, both at the sites of activation and distantly. Monocytes are innate immune cells with dynamic immune modulatory functions that change during the aging process, a phenomenon termed "inflammaging". We have previously shown that platelets are a major source of plasma beta-2 microglobulin (β2M) and that β2M induced a monocyte pro-inflammatory phenotype. Plasma β2M increases with age and is a pro-aging factor. We hypothesized that platelet derived β2M regulates monocyte phenotypes in the context of aging. Using wild-type (WT) and platelet specific β2M knockout mice (Plt-β2M-/-) mice, we found that plasma β2M increased with age and correlated with increased circulating Ly6C Hi monocytes. However, aged Plt-β2M-/mice had significantly fewer Ly6C Hi monocytes compared to WT mice. Quantitative real-time PCR of circulating monocytes showed that WT mouse monocytes were more "pro-inflammatory" with age, while Plt-β2M-/derived monocytes adopted a "pro-reparative" phenotype. Older Plt-β2M-/mice had a significant decline in heart function compared to age matched WT mice, as well as increased cardiac fibrosis and pro-fibrotic markers. These data suggest that platelet-derived β2M regulates age associated monocyte polarization, and a loss of platelet derived β2M shifted monocytes and macrophages to a pro-reparative phenotype and increased pro-fibrotic cardiac responses. Platelet regulation of monocyte phenotypes via β2M may maintain a balance between inflammatory and reparative signals that affects age related physiologic outcomes.

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“…C-reactive protein level was suggested to be inversely correlated to vaccine responsiveness in the elderly (95). Meanwhile, the absolute numbers of CD3 + , CD4 + , and CD8 + T cells in herpes zoster patients were significantly lower compared to those in the control (94). Given these findings, it will be important to further characterize age-associated changes in immune cell compartments in shingles patients on a larger scale.…”

Section: Vzvmentioning

confidence: 99%

“…The underlying mechanisms involved in VZV reactivation and susceptibility among the elderly or immunocompromised populations are currently unclear, although recent studies suggest aging cells as the cause of the inefficient clearance of virus-infected cells (91,92). Few markers that correlate with age-related severity in shingles or poor response to vaccination have also been identified (93)(94)(95). In particular, elderly residents in long-term care experience elevated incidence of shingles and post-herpetic neuralgia due to the high degree of immunosenescence, malnutrition, and existing chronic conditions.…”

Section: Vzvmentioning

confidence: 99%

Aging and the Immune System: the Impact of Immunosenescence on Viral Infection, Immunity and Vaccine Immunogenicity

2019

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Immunosenescence is characterized by a progressive deterioration of the immune system associated with aging. Multiple components of both innate and adaptive immune systems experience aging-related changes, such as alterations in the number of circulating monocytic and dendritic cells, reduced phagocytic activities of neutrophils, limited diversity in B/T cell repertoire, T cell exhaustion or inflation, and chronic production of inflammatory cytokines known as inflammaging. The elderly are less likely to benefit from vaccinations as preventative measures against infectious diseases due to the inability of the immune system to mount a successful defense. Therefore, aging is thought to decrease the efficacy and effectiveness of vaccines, suggesting aging-associated decline in the immunogenicity induced by vaccination. In this review, we discuss aging-associated changes in the innate and adaptive immunity and the impact of immunosenescence on viral infection and immunity. We further explore recent advances in strategies to enhance the immunogenicity of vaccines in the elderly. Better understanding of the molecular mechanisms underlying immunosenescencerelated immune dysfunction will provide a crucial insight into the development of effective elderly-targeted vaccines and immunotherapies.

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Decreased absolute numbers of CD3+ T cells and CD8+ T cells during aging in herpes zoster patients

Cited by 34 publications

References 35 publications

NKT-like cells reveal higher than T lymphocytes expression of cellular protective proteins HSP70 and SOD2 and comparably increased expression of SIRT1 in the oldest seniors

NKT-like cells reveal higher than T lymphocytes expression of cellular protective proteins HSP70 and SOD2 and comparably increased expression of SIRT1 in the oldest seniors

Platelet-derived β2m regulates age related monocyte/macrophage functions

Aging and the Immune System: the Impact of Immunosenescence on Viral Infection, Immunity and Vaccine Immunogenicity

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