Age-related aging of the immune system (4)
Between the death of immune cells and the activation of cytokine synthesis
Immuno senescence in aging: between immune cells depletion and cytokines up-regulation
Maria Teresa Ventura et al., Clinical and Molecular Allergy, 2017.
Translated by Evgenia Ryabtseva
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"Remodeling" of the immune system
The accumulation of reactive oxygen species leads to the fact that cells acquire resistance to apoptosis-induced damage and the number of cells that have entered the phase of physiological aging increases, while chronic antigenic stimulation induces an increase in the number of activated immune cells and excessive production of pro-inflammatory lymphokines that contribute to the remodeling of the immune system and the development of "inflamaging". Physiological aging is a highly dynamic phenomenon characterized by continuous adaptation of the body to destructive changes.
Reactive oxygen species are closely related to physiological aging and age-related diseases, in fact, genome instability caused by oxidative damage is the primary cause of aging. A low-calorie diet can increase the average level of the life-draining oxidative stress that accompanies normal metabolism.
As a result of both inflamaging and an increase in the level of reactive oxygen species, the mechanisms of modulating apoptosis in the process of physiological aging become especially unreliable. Decreased sensitivity to damage-induced apoptosis, characteristic of cells that have entered the phase of physiological aging, contributes to the accumulation of non-functional cells, CD8+ T-lymphocyte clones and memory cells, which reduces the resources of the immune system and increases the risk of infectious and neoplastic diseases, as well as degenerative disorders. An increase in the level of activation-induced apoptosis in response to the action of inflammatory cytokines contributes to: depletion of "naive" lymphocytes, a decrease in the ability of cells to clonal expansion, suppression of the reaction of T-lymphocytes with a decrease in the ability to maintain strong immune responses to antigenic stimuli and impoverishment of the range of immune defense mechanisms.
Shortening of telomeric DNA is associated with age and, regardless of genetic influence, is the result of the immunological history of each person with a close association between telomere length and mortality of people over the age of 65.
Apoptosis
Apoptosis is a complex complex of mechanisms of programmed cell death that ensures the maintenance of mechanisms of physiological homeostasis between survival and destruction of damaged cells, which prevents the development of many diseases, including neoplastic. Apoptosis is a strategic mechanism for the manifestation of clonotypic diversity in the process of selection of lymphocytes, providing control of clonal expansion after antigenic stimulation. Apoptosis can be induced by cellular damage (cell death induced by damage), and can also be activated by a sequence of signals and anchor ligands to the receptors of programmed cell death (cell death induced by activation). Apoptosis is a component of many changes characteristic of aging of the immune system, such as thymus involution, a change in the "repertoire" of T-lymphocytes and the accumulation of effector memory cells. All these events are prerequisites for the development of autoimmune diseases. Studies devoted to the study of apoptosis in aging have brought contradictory results. In fact, in the process of physiological aging, both apoptotic mechanisms can be modulated in different ways, which forms a different effect on the aging process. Proper modulation of this important function can increase life expectancy and suppress degenerative processes, as well as the development of inflammatory and neoplastic diseases, which are very characteristic of physiological aging.
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