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Lifestyle Factors in Cancer Survivorship
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
Although an inflammatory response is an important part of healthy immunity, persistent low-grade chronic inflammatory activity in plasma is associated with age-related diseases such as Alzheimer’s disease, atherosclerosis, and cancer. These are higher in overweight sedentary individuals, those with poor diets, type 2 diabetes, and the elderly.48 There is a general consensus that the reason for this stems from over-compensation by an ailing immune system trying to maintain immunosenescence. In these groups, poor IL-2 production leads to a decreased cytotoxic capacity of NK and T lymphocytes on a “per cell” basis. To compensate for this, higher levels of inflammatory biomarkers such as C-reactive protein, TNF, and interleukin-6 (IL-6), cytokine antagonists, and acute phase proteins are produced, which increase concentrations of NK cells and T cells. These inflammatory cytokines, however, also promote tumor development and growth directly or via prostaglandins (see below), which explains why they are associated with more advanced cancers and an increased risk of cancer-specific mortality.
Special Groups
Published in Vineet Relhan, Vijay Kumar Garg, Sneha Ghunawat, Khushbu Mahajan, Comprehensive Textbook on Vitiligo, 2020
Aging is associated with immunosenescence, seen as a documented decrease in immune response to specific antigens. However, there is a paradoxical increase in the incidence of autoimmune diseases in the aged population, probably owing to a decreased clearance of accumulated protein antigens. This observation could explain the pathogenesis of late-onset vitiligo. At the same time, aging is also associated with melanocyte senescence, leading to a decrease in the number of melanocytes on photo-exposed as well as photoprotected skin. This decrease is approximately 10%–20% over a decade. Whether this factor contributes to late-onset vitiligo is, however, unclear [1].
The aging body
Published in Jennifer R. Sasser, Harry R. Moody, Gerontology, 2018
Jennifer R. Sasser, Harry R. Moody
A related phenomenon is the role of inflammation in tissues. Chronic, low-grade inflammation is known to be closely linked to the diseases associated with aging and perhaps even with biological aging itself, but it is not clear what is the cause or effect here. To speak of “immunosenescence” is to emphasize that the inflammatory response of the body is tightly controlled by our immune system in all its complexity. There are multiple control systems involved here, and the study of inflammation has become central to current research in the biology of aging.
An immunologist’s guide to immunosenescence and its treatment
Published in Expert Review of Clinical Immunology, 2022
Calogero Caruso, Mattia Emanuela Ligotti, Giulia Accardi, Anna Aiello, Giuseppina Candore
This type of treatment might be potentially available soon thanks to cytomics technologies that are beginning to provide powerful tools that allow the analysis of a huge number of parameters simultaneously, in a single cell, both from the phenotypic and from the genetic and transcriptomic point of view. This simultaneous analysis will allow to define more precise aspects of immunosenescence, obtaining a highly reliable ‘immunological score’ with prognostic value. In addition, an effort should be made in terms of selection and recruitment of older subjects, with careful collection of demographic, clinical, and behavioral data, to correlate the immunological profile with successful or unsuccessful aging. Particular attention should be paid to the recruitment of semi and super-centenarians as well as centenarians as an example of positive biology. However, the present review shows how appreciable results in the modification of immunosenescence biomarkers can be achieved with lifestyle modification.
Non-contact infrared assessment of human body temperature: The journal Temperature toolbox
Published in Temperature, 2021
Josh Foster, Alex Bruce Lloyd, George Havenith
Immunosenescence refers to the gradual deterioration of the immune system brought on by natural aging [42]. In the context of fever, aging decreases endotoxin-induced production of prostaglandin E2 (PGE2) in the hypothalamus, and PGE2 initiates the thermoregulatory response to infection [43]. Consequently, aging (typically over 65 years) impacts the ability of humans to mount a febrile response to infection, which reduces the peak Tcore attained [44–46]. Recent evidence supports lower Tcore thresholds for COVID-19 screening in nursing homes [47], suggesting that a “one size fits all” threshold temperature is not optimal for all age groups. However, there exists a lack of evidence relating to how the threshold temperature varies with aging i.e., is there a linear or exponential reduction in maximum febrile Tcore, and how does this vary based on the pathogen and dose. More research is required to generate an age adjusted temperature threshold but is an important avenue for future work.
The epidemiologic and biologic basis for classifying older age as a high-risk, immunocompromising condition for pneumococcal vaccine policy
Published in Expert Review of Vaccines, 2021
Lindsay R. Grant, Mary P. E. Slack, Qi Yan, Krzysztof Trzciński, Jane Barratt, Elizabeth Sobczyk, James Appleby, Alejandro Cané, Luis Jodar, Raul E. Isturiz, Bradford D. Gessner
In this context, the purpose of this review is to provide a rationale and framework for including older age – based on the process of immunosenescence – as an immunocompromising condition for the purposes of pneumococcal vaccine recommendations. In principle, immunosenescence itself could be included as an immunocompromising condition. However, in practice no marker exists currently to identify persons that have reached specific levels of immunosenescence, and consequently we propose that older age be used as a surrogate. In support of this categorization, we will review the biologic evidence pertaining to pneumococcal disease risk in older adults. We then will review the epidemiologic evidence supporting that older age may confer pneumococcal disease risk similar to that of immunocompromising conditions already considered as high-risk for pneumococcal disease. We acknowledge that the epidemiologic evidence presented herein derives from countries that may have a pneumococcal vaccination policy already in place for older adults. However, none have adopted the framework we propose here. Acceptance and application of this framework would demonstrate a consistent approach to pneumococcal vaccine recommendations across the lifespan based on the available evidence for risk of pneumococcal disease. This would thereby facilitate decision-making by national vaccine technical committees (VTCs) and clinicians regardless of the adult pneumococcal vaccination policy that is selected for a particular country.