Age-associated immune deficiency is found in both long- and short-lived species as a function of their age relative to life expectancy rather than elapsed time.
Thymic involution is common in most mammals; in humans it begins after puberty, as the immunological defense against most novel antigens is necessary mainly during infancy and childhood.
[5] It is believed that the conversion to memory phenotype can be accelerated by restimulation of the immune system by persistent pathogens such as CMV and HSV.
[5] Such a distribution shift leads to increased susceptibility to non-persistent infection, cancer, autoimmune diseases, cardiovascular health conditions and many others.
[13][14] T cells are not the only immune cells affected by aging: In addition to changes in immune responses, the beneficial effects of inflammation devoted to the neutralisation of dangerous and harmful agents early in life and in adulthood become detrimental late in life in a period largely not foreseen by evolution, according to the antagonistic pleiotropy theory of aging.
[9] The elderly frequently present with non-specific signs and symptoms, and clues of focal infection are often absent or obscured by chronic conditions.
The reduced efficacy of vaccination in the elderly stems from their restricted ability to respond to immunization with novel non-persistent pathogens, and correlates with both CD4:CD8 alterations and impaired dendritic cell function.
Coenzyme NAD+ is reduced in various tissues in an age-dependent manner, and thus redox potential associated changes seem to be critical in the aging process,[55] and NAD+ supplements may have protective effects.