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Bio-Rad Immune Senescence and Inflammaging

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Immune Senescence and Inflammaging


The last 50 years have seen a steady increase in life expectancy across the developed world mainly due to disease prevention, improved hygiene, and nutrition. However with increasing age, a new problem has appeared - the phenomenon of inflammaging and immune senescence. This is now a focus for research as the decline in immune parameters which can lead to disabilities and poor health in an aging population, has significant impact on social welfare.

Inflammaging is a hallmark of virtually every major age-related disease and phenotype such as dementia, Parkinson’s disease, atherosclerosis, type 2 diabetes, cancer, and arthritis, and is a pathological characteristic of aging tissues found across multiple species (Xu and Larbi 2017).

Inflammaging Definition and Hallmarks

Inflammaging refers to low levels of chronic inflammation that progressively increase with age. It is thought to be due to the age-related accumulation of senescent cells (here senescent meaning old) which do not proliferate. This is theorized, in part, due to resistance to apoptosis induced damage and not T cell exhaustion. Inflammaging is characterized by low level persistent infiltration of immune cells, primarily but not exclusively, cells of the innate immune system and elevated levels of pro-inflammatory cytokines, and chemokines. With age, this low grade inflammation leads to a counter-regulation of anti-inflammatory molecules. Cells of both the innate and adaptive immune compartments can change with age, becoming senescent. It is not clear why this happens, but may be as a result of sustained activation in the absence of specific challenge and persistence of memory, even in the innate immune compartment (Ventura et al. 2017).