Abstract
SummaryIt is widely accepted that aging is accompanied by remodelling of the immune system including thymic atrophy and increased frequency of senescent T cells, leading to immune compromise. However, physical activity, which influences immunity but declines dramatically with age, is not considered in this literature. We assessed immune profiles in 125 adults (55–79 years) who had maintained a high level of physical activity (cycling) for much of their adult lives, 75 age‐matched older adults and 55 young adults not involved in regular exercise. The frequency of naïve T cells and recent thymic emigrants (RTE) were both higher in cyclists compared with inactive elders, and RTE frequency in cyclists was no different to young adults. Compared with their less active counterparts, the cyclists had significantly higher serum levels of the thymoprotective cytokine IL‐7 and lower IL‐6, which promotes thymic atrophy. Cyclists also showed additional evidence of reduced immunesenescence, namely lower Th17 polarization and higher B regulatory cell frequency than inactive elders. Physical activity did not protect against all aspects of immunesenescence: CD28−ve CD57+ve senescent CD8 T‐cell frequency did not differ between cyclists and inactive elders. We conclude that many features of immunesenescence may be driven by reduced physical activity with age.
Highlights
Aging is accompanied by a decline in immune competence, termed immunesenescence, which is characterized by an increased risk of infections and chronic inflammatory diseases, poor vaccine efficacy, failure to maintain immunity to latent infections such as Varicella Zoster and increased autoimmunity (DiCarlo, Fuldner, Kaminski & Hodes, 2009; Montecino-Rodriguez, Berent-Maoz & Dorshkind, 2013)
Immune cell phenotype was determined in peripheral blood mononuclear cells (PBMC)
This decline was not seen in the master cyclists as their T-cell frequency was higher than the inactive elders, p = .0003 (Figure 1a) and not different from the young adults
Summary
Aging is accompanied by a decline in immune competence, termed immunesenescence, which is characterized by an increased risk of infections and chronic inflammatory diseases, poor vaccine efficacy, failure to maintain immunity to latent infections such as Varicella Zoster and increased autoimmunity (DiCarlo, Fuldner, Kaminski & Hodes, 2009; Montecino-Rodriguez, Berent-Maoz & Dorshkind, 2013). The mechanisms underlying this compromised immunity include involution of the thymus, which begins in early adulthood in humans and accelerates rapidly after 40 years of age (Mitchell, Lang & Aspinall, 2010).
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