Macrophages of the innate immune system take on different states known as polarizations depending on their duties. M1 macrophages are aggressive and inflammatory, involved in the destruction of pathogens and harmful cells. M2 macrophages aid in the processes of regeneration. The immune system becomes more inflammatory with advancing age. This chronic inflammation drives progression of most of the common age-related diseases, and an excess of M1 macrophages appears as a feature of many of those conditions. The research community is looking into ways to force more macrophages into the M2 polarization, as a possible approach to override a fraction of age-related immune dysfunction. In this context, researchers here report on their evaluation of differences in the macrophage population between more and less healthy older individuals.
The low-grade, chronic inflammatory state affecting aging organisms – inflammaging – is among the major risk factors for the development of the most common human age-related diseases (ARDs). Increasing evidence suggests that inflammaging is underpinned by monocytes/macrophages, while the acquisition of a senescent phenotype – a phenomenon that has been defined as macroph-aging – impairs the ability of immune cells to cope with stressors, thus
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