Physical Activity and Diet Shape the Immune System During Aging
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Markers of T Cell Senescence in Humans
International Journal of Molecular Sciences Review Markers of T Cell Senescence in Humans Weili Xu 1,2 and Anis Larbi 1,2,3,4,5,* 1 Biology of Aging Program and Immunomonitoring Platform, Singapore Immunology Network (SIgN), Agency for Science Technology and Research (A*STAR), Immunos Building, Biopolis, Singapore 138648, Singapore; [email protected] 2 School of Biological Sciences, Nanyang Technological University, Singapore 637551, Singapore 3 Department of Microbiology, National University of Singapore, Singapore 117597, Singapore 4 Department of Geriatrics, Faculty of Medicine, University of Sherbrooke, Sherbrooke, QC J1K 2R1, Canada 5 Faculty of Sciences, University ElManar, Tunis 1068, Tunisia * Correspondence: [email protected]; Tel.: +65-6407-0412 Received: 31 May 2017; Accepted: 26 July 2017; Published: 10 August 2017 Abstract: Many countries are facing the aging of their population, and many more will face a similar obstacle in the near future, which could be a burden to many healthcare systems. Increased susceptibility to infections, cardiovascular and neurodegenerative disease, cancer as well as reduced efficacy of vaccination are important matters for researchers in the field of aging. As older adults show higher prevalence for a variety of diseases, this also implies higher risk of complications, including nosocomial infections, slower recovery and sequels that may reduce the autonomy and overall quality of life of older adults. The age-related effects on the immune system termed as “immunosenescence” can be exemplified by the reported hypo-responsiveness to influenza vaccination of the elderly. T cells, which belong to the adaptive arm of the immune system, have been extensively studied and the knowledge gathered enables a better understanding of how the immune system may be affected after acute/chronic infections and how this matters in the long run. -
Remodeling of the Immune Response with Aging: Immunosenescence and Its Potential Impact on COVID-19 Immune Response
REVIEW published: 07 August 2020 doi: 10.3389/fimmu.2020.01748 Remodeling of the Immune Response With Aging: Immunosenescence and Its Potential Impact on COVID-19 Immune Response Lucas Leite Cunha 1, Sandro Felix Perazzio 2, Jamil Azzi 3, Paolo Cravedi 4 and Leonardo Vidal Riella 5,6* 1 Department of Medicine, Escola Paulista de Medicina, Federal University of São Paulo, São Paulo, Brazil, 2 Division of Rheumatology, Escola Paulista de Medicina, Federal University of São Paulo, São Paulo, Brazil, 3 Schuster Transplantation Research Center, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, United States, 4 Renal Division, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, United States, 5 Division of Nephrology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States, 6 Department of Surgery, Center for Transplantation Sciences, Massachusetts General Hospital, Boston, MA, United States Elderly individuals are the most susceptible to an aggressive form of coronavirus disease Edited by: Massimo Triggiani, (COVID-19), caused by SARS-CoV-2. The remodeling of immune response that is University of Salerno, Italy observed among the elderly could explain, at least in part, the age gradient in lethality of Reviewed by: COVID-19. In this review, we will discuss the phenomenon of immunosenescence, which Sebastiano Gangemi, University of Messina, Italy entails changes that occur in both innate and adaptive immunity with aging. Furthermore, Remo Castro Russo, we will discuss inflamm-aging, a low-grade inflammatory state triggered by continuous Federal University of Minas antigenic stimulation, which may ultimately increase all-cause mortality. In general, the Gerais, Brazil elderly are less capable of responding to neo-antigens, because of lower naïve T cell *Correspondence: Leonardo Vidal Riella frequency. -
Brain Inflammaging: Roles of Melatonin, Circadian Clocks
C al & ellu ic la n r li Im C m Journal of Clinical & Cellular f u o n l o a l n o Hardeland, J Clin Cell Immunol 2018, 9:1 r g u y o J Immunology DOI: 10.4172/2155-9899.1000543 ISSN: 2155-9899 Mini Review Open Access Brain Inflammaging: Roles of Melatonin, Circadian Clocks and Sirtuins Rüdiger Hardeland* Johann Friedrich Blumenbach Institute of Zoology and Anthropology, University of Göttingen, Göttingen, Germany *Corresponding author: Rüdiger Hardeland, Johann Friedrich Blumenbach Institute of Zoology and Anthropology, Bürgerstrasse. 50, D-37073 Göttingen, Germany, Tel: +49-551-395414; E-mail: [email protected] Received date: February 13, 2018; Accepted date: February 26, 2018; Published date: February 28, 2018 Copyright: ©2018 Hardeland R. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium. Abstract Inflammaging denotes the contribution of low-grade inflammation to aging and is of particular importance in the brain as it is relevant to development and progression of neurodegeneration and mental disorders resulting thereof. Several processes are involved, such as changes by immunosenescence, release of proinflammatory cytokines by DNA-damaged cells that have developed the senescence-associated secretory phenotype, microglia activation and astrogliosis because of neuronal overexcitation, brain insulin resistance, and increased levels of amyloid-β peptides and oligomers. Melatonin and sirtuin1, which are both part of the circadian oscillator system share neuroprotective and anti-inflammatory properties. In the course of aging, the functioning of the circadian system deteriorates and levels of melatonin and sirtuin1 progressively decline. -
Cellular Senescence: Friend Or Foe to Respiratory Viral Infections?
Early View Perspective Cellular Senescence: Friend or Foe to Respiratory Viral Infections? William J. Kelley, Rachel L. Zemans, Daniel R. Goldstein Please cite this article as: Kelley WJ, Zemans RL, Goldstein DR. Cellular Senescence: Friend or Foe to Respiratory Viral Infections?. Eur Respir J 2020; in press (https://doi.org/10.1183/13993003.02708-2020). This manuscript has recently been accepted for publication in the European Respiratory Journal. It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJ online. Copyright ©ERS 2020. This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial Licence 4.0. Cellular Senescence: Friend or Foe to Respiratory Viral Infections? William J. Kelley1,2,3 , Rachel L. Zemans1,2 and Daniel R. Goldstein 1,2,3 1:Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA 2:Program in Immunology, University of Michigan, Ann Arbor, MI, USA 3:Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI USA Email of corresponding author: [email protected] Address of corresponding author: NCRC B020-209W 2800 Plymouth Road Ann Arbor, MI 48104, USA Word count: 2750 Take Home Senescence associates with fibrotic lung diseases. Emerging therapies to reduce senescence may treat chronic lung diseases, but the impact of senescence during acute respiratory viral infections is unclear and requires future investigation. Abstract Cellular senescence permanently arrests the replication of various cell types and contributes to age- associated diseases. -
Immunosenescence in Neurocritical Care Shigeaki Inoue*, Masafumi Saito and Joji Kotani
Inoue et al. Journal of Intensive Care (2018) 6:65 https://doi.org/10.1186/s40560-018-0333-5 REVIEW Open Access Immunosenescence in neurocritical care Shigeaki Inoue*, Masafumi Saito and Joji Kotani Abstract Background: Several advanced and developing countries are now entering a superaged society, in which the percentage of elderly people exceeds 20% of the total population.Insuchanagingsociety,thenumberofage-related diseases such as malignant tumors, diabetes, and severe infections including sepsis is increasing, and patients with such disorders often find themselves in the ICU. Main body: Age-related diseases are closely related to age-induced immune dysfunction, by which reductions in the efficiency and specificity of the immune system are collectively termed “immunosenescence.” The most noticeable is a decline in the antigen-specific acquired immune response. The exhaustion of T cells in elderly sepsis is related to an increase in nosocomial infections after septicemia, and even death over subacute periods. Another characteristic is that senescent cells that accumulate in body tissues over time cause chronic inflammation through the secretion of proinflammatory cytokines, termed senescence-associated secretory phenotype. Chronic inflammation associated with aging has been called “inflammaging,” and similar age-related diseases are becoming an urgent social problem. Conclusion: In neuro ICUs, several neuro-related diseases including stroke and sepsis-associated encephalopathy are related to immunosenescence and neuroinflammation in the elderly. Several advanced countries with superaged societies face the new challenge of improving the long-term prognosis of neurocritical patients. Keywords: Sepsis, Elderly, Immunosenescence, Immune paralysis Background What is the immune system? Japan is facing the social problem of a declining birth rate Immunity is the means by which multicellular organisms and an aging population, in which it is estimated that resist the attacks of harmful invading microorganisms. -
Cell Death and Ageing – a Question of Cell Type
Opinion TheScientificWorldJOURNAL (2002) 2, 943–948 ISSN 1537-744X; DOI 10.1100/tsw.2002.163 Cell Death and Ageing – A Question of Cell Type Pidder Jansen-Dürr Institute for Biomedical Ageing Research, Rennweg 10, 6020 Innsbruck, Austria Received December 19, 2001; Revised February 6, 2002; Accepted February 11, 2002; Published April 9, 2002 Replicative senescence of human cells in primary culture is a widely accepted model for studying the molecular mechanisms of human ageing. The standard model used for studying human ageing consists of fibroblasts explanted from the skin and grown into in vitro senescence. From this model, we have learned much about molecular mechanisms underlying the human ageing process; however, the model presents clear limitations. In particular, a long-standing dogma holds that replicative senescence involves resistance to apoptosis, a belief that has led to considerable confusion concerning the role of apoptosis during human ageing. While there are data suggesting that apoptotic cell death plays a key role for ageing in vivo and in the pathogenesis of various age-associated diseases, this is not reflected in the current literature on in vitro senescence. In this article, I summarize key findings concerning the relationship between apoptosis and ageing in vivo and also review the literature concerning the role of apoptosis during in vitro senescence. Recent experimental findings, summarized in this article, suggest that apoptotic cell death (and probably other forms of cell death) are important features of the ageing process that can also be recapitulated in tissue culture systems to some extent. Another important lesson to learn from these studies is that mechanisms of in vitro senescence differ considerably between various histotypes. -
Age-Related Cerebral Small Vessel Disease and Inflammaging
Li et al. Cell Death and Disease (2020) 11:932 https://doi.org/10.1038/s41419-020-03137-x Cell Death & Disease REVIEW ARTICLE Open Access Age-related cerebral small vessel disease and inflammaging Tiemei Li1,2,YinongHuang1,3,WeiCai1,2, Xiaodong Chen1,2, Xuejiao Men1,2, Tingting Lu1,2, Aiming Wu1,2 and Zhengqi Lu 1,2 Abstract The continued increase in global life expectancy predicts a rising prevalence of age-related cerebral small vessel diseases (CSVD), which requires a better understanding of the underlying molecular mechanisms. In recent years, the concept of “inflammaging” has attracted increasing attention. It refers to the chronic sterile low-grade inflammation in elderly organisms and is involved in the development of a variety of age-related chronic diseases. Inflammaging is a long-term result of chronic physiological stimulation of the immune system, and various cellular and molecular mechanisms (e.g., cellular senescence, immunosenescence, mitochondrial dysfunction, defective autophagy, metaflammation, gut microbiota dysbiosis) are involved. With the deepening understanding of the etiological basis of age-related CSVD, inflammaging is considered to play an important role in its occurrence and development. One of the most critical pathophysiological mechanisms of CSVD is endothelium dysfunction and subsequent blood-brain barrier (BBB) leakage, which gives a clue in the identification of the disease by detecting circulating biological markers of BBB disruption. The regional analysis showed blood markers of vascular inflammation are often associated with deep perforating arteriopathy (DPA), while blood markers of systemic inflammation appear to be associated with cerebral amyloid angiopathy (CAA). Here, we discuss recent findings in the pathophysiology of inflammaging and their effects on the development of age-related CSVD. -
Retinal Inflammaging: Pathogenesis and Prevention
Vol 4, Issue 4, 2016 ISSN - 2321-4406 Review Article RETINAL INFLAMMAGING: PATHOGENESIS AND PREVENTION ABHA PANDIT1, DEEPTI PANDEY BAHUGUNA2, ABHAY KUMAR PANDEY3*, PANDEY BL4, S Pandit5 1Department of Medicine, Index Medical College Hospital and Research Centre, Indore, Madhya Pradesh, India. 2Consultant, Otorhinolaryngologist, Shri Laxminarayan Marwari Multispeciality Charity Hospital, Varanasi, Uttar Pradesh, India. 3Department of Physiology, Government Medical College, Banda, Uttar Pradesh, India. 4Department of Pharmacology, IMS, Banaras Hindu University, Varanasi, Uttar Pradesh, India. 5Department of Ophthalmology, Health Services, Indore, Madhya Pradesh, India. Email: [email protected] Received: 09 June 2016, Revised and Accepted: 14 June 2016 ABSTRACT Macula lutea, the yellow spot or fovea centralis in eye, serves the distinctive central vision in perceiving visual cues and contributing to task performance. Impaired visual acuity, in later years in life, compromises safety, productivity, and life quality. Carotenoid pigment content declines with cumulation of light-induced damage through aging process in the retina. The progression of resultant macular degeneration is aggravated by oxidative stress, inflammation, raised blood sugar, and vasculopathy associating aging. Senescent dry degeneration involves drusen (a compound of glycolipid and glycol-conjugate core) deposition that impairs metabolic connectivity of upper layers of retina with choroid. Degeneration of retinal pigment epithelium and photoreceptors thus results. The late more severe form of age-related macular degeneration (AMD), involves factors inducing choroidal neovascularization. Leaky neocapillaries speed degenerative process of the retina. Most age-related pathologies are initiated by metabolic disruptions and AMD shares features of systemic atherosclerosis. An aberrant tissue response to free radical stress, vasculopathy, and local ischemic underlies AMD pathogenesis. -
Cellular Senescence and Inflammaging in the Skin Microenvironment
International Journal of Molecular Sciences Review Cellular Senescence and Inflammaging in the Skin Microenvironment Young In Lee 1,2 , Sooyeon Choi 1, Won Seok Roh 1 , Ju Hee Lee 1,2,* and Tae-Gyun Kim 1,* 1 Department of Dermatology, Severance Hospital, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul 107-11, Korea; [email protected] (Y.I.L.); [email protected] (S.C.); [email protected] (W.S.R.) 2 Scar Laser and Plastic Surgery Center, Yonsei Cancer Hospital, Yonsei University College of Medicine, Seoul 107-11, Korea * Correspondence: [email protected] (J.H.L.); [email protected] (T.-G.K.); Tel.: +82-2-2228-2080 (J.H.L. & T.-G.K.) Abstract: Cellular senescence and aging result in a reduced ability to manage persistent types of inflammation. Thus, the chronic low-level inflammation associated with aging phenotype is called “inflammaging”. Inflammaging is not only related with age-associated chronic systemic diseases such as cardiovascular disease and diabetes, but also skin aging. As the largest organ of the body, skin is continuously exposed to external stressors such as UV radiation, air particulate matter, and human microbiome. In this review article, we present mechanisms for accumulation of senescence cells in different compartments of the skin based on cell types, and their association with skin resident immune cells to describe changes in cutaneous immunity during the aging process. Keywords: inflammaging; senescence; skin; fibroblasts; keratinocytes; melanocytes; immune cells Citation: Lee, Y.I.; Choi, S.; Roh, W.S.; Lee, J.H.; Kim, T.-G. Cellular Senescence and Inflammaging in the 1. -
Does the Immune System Grow Old Gracefully?
Immunology Does the immune system grow old gracefully? Donald B. Palmer ‘You don’t stop laughing when you grow old, you grow old when you stop laughing’. and Tamar Freiberger George Bernard Shaw Downloaded from http://portlandpress.com/biochemist/article-pdf/41/1/26/851497/bio041010026.pdf by guest on 27 September 2021 (Royal Veterinary College, University of London, UK) The immune system consists of an array of cells and Making T cells can be exhausting soluble factors that are designed to protect the host from pathogens and infectious diseases, and therefore T cells represent a key component of the immune system; represents a vital entity for an organism’s survival. they are able to directly remove pathogens as well as Moreover, with increasing age, the immune system coordinate other elements of the immune system to elicit undergoes dramatic changes resulting in a decline in their function. A large number of studies have suggested immune function, which is seen in humans as well as in that a progressive decline in T cell function is one of the many other species. Such changes, collectively termed major factors that contributes to the clinical features of immunosenescence, often lead to increased susceptibility immunosenescence. T cells are derived from haematopietic and severity of infections, cancers and autoimmune stem cells (HSCs), however for HSCs to become T cells diseases, together with the reduced ability to respond they are required to enter the thymus (a primary lymphoid to vaccination, which is often seen in older individuals. organ) and in the presence of appropriate signals, provided Given the direct correlation between immune function by the thymic environment, differentiate into T cells. -
Immunosenescence in B Cells: a Study on Changes in Immunoregulator Expression and Metabolism with Age
University of Pennsylvania ScholarlyCommons Publicly Accessible Penn Dissertations 2015 Immunosenescence in B Cells: A Study on Changes in Immunoregulator Expression and Metabolism With Age Senthil Kannan University of Pennsylvania, [email protected] Follow this and additional works at: https://repository.upenn.edu/edissertations Part of the Allergy and Immunology Commons, Cell Biology Commons, Immunology and Infectious Disease Commons, and the Medical Immunology Commons Recommended Citation Kannan, Senthil, "Immunosenescence in B Cells: A Study on Changes in Immunoregulator Expression and Metabolism With Age" (2015). Publicly Accessible Penn Dissertations. 1802. https://repository.upenn.edu/edissertations/1802 This paper is posted at ScholarlyCommons. https://repository.upenn.edu/edissertations/1802 For more information, please contact [email protected]. Immunosenescence in B Cells: A Study on Changes in Immunoregulator Expression and Metabolism With Age Abstract There is a vital need for better vaccines for the aging population, and especially better vaccines to influenza viruses. oT address this, I studied immunosenescence in B cells and antibody secreting cells (ASCs) in mice and humans. In humans, I measured humoral immune responses to the trivalent inactivated influenza accinev (TIV) during the 2011-12 and 2012-13 influenza seasons. ASCs in the aged were observed to have decreased expression of the defining markers CD27 and CD38. Aged ASCs also expressed lower levels of B and T Lymphocyte attenuator (BTLA) on their surface. Expression of BTLA inversely correlated with age and appeared to be linked to shifting the nature of the response from IgM to IgG. High BTLA expression on mature B cells was linked to higher IgG responses to the H1N1 virus. -
Immunosenescence of Lymphocytes T and Implications for Age-Related Disorders
Immunosenescence of Lymphocytes T and Implications for Age-Related Disorders Anna Tylutka University of Zielona Góra Barbara Morawin University of Zielona Góra Artur Gramacki University of Zielona Góra Agnieszka Zembron-Lacny ( [email protected] ) University of Zielona Góra Research Keywords: fat content, ow cytometry, gender, health status, immune ageing Posted Date: April 29th, 2020 DOI: https://doi.org/10.21203/rs.3.rs-24968/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 1/18 Abstract Background. The decrease in immunity with age is still a major health concern as elderly people are more susceptible to infections and increased incidence of autoimmunity. Consequently, there is an increasing interest in immunosenescence and changes in immunology cells like T cells. The aim of our study was to nd a disproportion in subpopulation of T cells as well as CD4/CD8 ratio depending on the age, gender or comorbidities. Results. In the present study, a ow cytometry was used to indicate the differences between age, sex, disorders and fat content in the CD4+ and CD8+ T cells population divided into naïve and memory cells as well as CD4/CD8 ratio in people aged 71.9± 5.8 years (females n=83, males n=16) compared to young people aged 20.6 ± 1.1 years (females n=12, males n=19). The percentage of naïve CD4+ and CD8+ cells was found to be statistically signicantly lower in the elderly compared to the young. In addition, gender was observed to play an important role in the outcomes in the analysed subpopulations and in female group, who live statistically longer than males, our older group of Polish women demonstrated a signicantly higher percentage of naïve lymphocytes in both the CD4+ and CD8+ populations compared to men.