2011
DOI: 10.1097/jes.0b013e318201f39d
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Aging, Persistent Viral Infections, and Immunosenescence

Abstract: Overcrowding the immune space with excess clones of viral-specific T cells causes the naïve T-cell repertoire to shrink, which increases infection susceptibility to novel pathogens. Physical exercise preferentially mobilizes senescent T cells from the peripheral tissues into the blood, which might facilitate their subsequent apoptosis and create "vacant space" for newly functional T cells to occupy and expand the naïve T-cell repertoire.

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Cited by 127 publications
(146 citation statements)
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“…For example, it has been shown that symptoms of URTI in swimmers were positively associated with previous Epstein-Barr viral infection and partially with viral shedding (Gleeson et al, 2002). Furthermore, there is increasing evidence that infection history has a strong influence on cellular immune responses to exercise (Turner et al, 2010;Simpson et al, 2011).…”
Section: Background and Evidencementioning
confidence: 99%
“…For example, it has been shown that symptoms of URTI in swimmers were positively associated with previous Epstein-Barr viral infection and partially with viral shedding (Gleeson et al, 2002). Furthermore, there is increasing evidence that infection history has a strong influence on cellular immune responses to exercise (Turner et al, 2010;Simpson et al, 2011).…”
Section: Background and Evidencementioning
confidence: 99%
“…Antigenexperienced T cells that have reached end-stage replication develop an increased resistance to apoptosis (Spaulding et al 1999), allowing them to accumulate in blood and tissues at the expense of naïve antigen-virgin T cells, increasing host infection risk. This is due to a lowered "immune space" that is caused by the shrunken repertoire of naïve T cells that are capable of responding to newly evolving pathogens such as inXuenza, rhinovirus (the common cold) and respiratory syncytial virus (RSV) among others (Koch et al 2006;Pawelec et al 2009;Simpson 2011;Simpson and Guy 2010).…”
Section: Introductionmentioning
confidence: 99%
“…T-cell senescence is a state of immune dysfunction whereby antigen-speciWc T cells become terminally diVerentiated and are unable to proliferate in response to further antigenic stimuli (Simpson 2011;Simpson and Guy 2010). Persistent exposure to pathogens, frequent reactivations of latent viruses and increased levels of oxidative stress are believed to cause the premature senescence of speciWc T-cell subsets (EVros 2010;Pawelec et al 2009).…”
Section: Introductionmentioning
confidence: 99%
“…12 Each response to a pathogenic challenge results in a further modulation of the adaptive immune system. 13 Once adulthood is reached, the adaptive and innate immune systems are fully developed and generally considered to be robust. 14 A decline in cellular and humoral immune function has been noted in older adults.…”
Section: The Immune Systemmentioning
confidence: 99%
“…16 Immunosenscence is characterized by impaired function of immune cell populations and an ''overcrowding'' of the so-called immune space whereby the population of leukocyte subsets essential in responses to novel pathogens (naïve T lymphocytes), have been gradually replaced by expanded clones (effector and effector-memory T lymphocytes) that have a late-stage differentiation phenotype and limited antigenic specificity. 13,15,[17][18][19] An increased inflammatory status has also been associated with the ageing process (inflamm-aging) which may give rise to other health issues in the older population (cardiovascular disease , Type 2 diabetes). 20 Immunosenescence is a primary factor contributing to increased infection susceptibility and decreased response to vaccinations in the elderly.…”
Section: The Immune Systemmentioning
confidence: 99%