Immunosenescence

Source: Wikipedia, the free encyclopedia.

Immunosenescence is the gradual deterioration of the

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.[2]

It has been studied in animal models including mice, marsupials and monkeys.

exhaustion, immunosenescence belongs among the major immune system dysfunctional states. However, while T-cell anergy is a reversible condition, as of 2020 no techniques for immunosenescence reversal had been developed.[6][7]

Immunosenescence is not a random deteriorative phenomenon, rather it appears to inversely recapitulate an evolutionary pattern. Most of the parameters affected by immunosenescence appear to be under genetic control.

Age-associated decline in immune function

Aging of the immune system is a controversial phenomenon. Senescence refers to

replicative senescence from cell biology, which describes the condition when the upper limit of cell divisions (Hayflick limit) has been exceeded, and such cells commit apoptosis or lose their functional properties. Immunosenescence generally means a robust shift in both structural and functional parameters that has a clinically relevant outcome.[10] Thymus involution is probably the most relevant factor responsible for immunosenescence. 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.[11]

The major characteristic of the immunosenescent

persistent pathogens such as CMV and HSV. By age 40, an estimated 50% to 85% of adults have contracted human cytomegalovirus (HCMV).[1] Recurring infections by latent herpes viruses can exhaust the immune system of elderly persons.[12] Consistent, repeated stimulation by such pathogens leads to preferential differentiation of the T-cell memory phenotype, and a 2020 review reported that CD8+ T-cell precursors, specific for the most rare and less frequently present antigens shed the most.[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

macrophages become dysregulated as a consequence of environmental changes.[26]

T-cell biomarkers of age-dependent dysfunction

T cells' functional capacity is most influenced by aging effects. Age-related alterations are evident in all T-cell development stages, making them a significant factor in immunosenescence.

thymocytes (i.e. immature T cells), thus reducing peripheral naïve T cell output.[30][31] Once matured and circulating throughout the peripheral system, T cells undergo deleterious age-dependent changes. This leaves the body practically devoid of virgin T cells, which makes it more prone to a variety of diseases.[9]

Challenges

The elderly frequently present with non-specific signs and symptoms, and clues of focal infection are often absent or obscured by chronic conditions.[2] This complicates diagnosis and treatment.

Vaccination in the elderly

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.[48] Therefore, vaccination in earlier life stages seems more likely to be effective, although the duration of the effect varies by pathogen.[49][10]

Rescue of the advanced-age phenotype

Removal of senescent cells with

senolytic compounds has been proposed as a method of enhancing immunity during aging.[50]

Immune system aging in mice can be partly restricted by restoring thymus growth, which can be achieved by transplantation of proliferative thymic epithelial cells from young mice.

Rapamycin, an antitumor and immunosuppresant, acts similarly.[57]

References