Telomeres are protein-DNA complexes located at the ends of linear chromosomes and consist of short, tandem G-rich hexanucleotide repeats and associated proteins.
Their length shortens with each cell division and correlates inversely with age.
It can be modified by genetic and epigenetic factors, sex hormones, reactive oxygen species and inflammatory reactions.
A critical minimum length of telomeres triggers cell cycle arrest or aging of the cell.
The immune system is very sensitive to telomere shortening because its competence strictly depends on cell renewal and clonal expansion of T and B cell populations.
Cells of the immune system are unique among normal somatic cells in their ability to upregulate telomerase, the telomere-lengthening enzyme, and limit telomere shortening in the process of cell proliferation that occurs in activated cells.
Telomere length is highly variable in humans. Lineage-specific telomere shortening with different kinetics of telomere wear has been observed in CD4+, CD8+ T lymphocytes, B lymphocytes, granulocytes, monocytes and NK cell populations. Immunosenescence is characterized by a specific remodeling of the immune system induced by antigen exposure and oxidative stress.
As the immune system ages, adaptive immunity deteriorates due to a progressive decline in naive T and B cells and a decrease in the absolute number of T and B lymphocytes.
The innate compartment of the immune system is relatively well preserved, although some age-related changes can also be observed. Nonagenarians or centenarians represent a phenomenon of successful aging of the immune system, as most of their immune parameters are well preserved.
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