Department of Genetics, Physiology, and Microbiology (Unit of Animal Physiology), Faculty of Biology, Complutense University of Madrid, 28040 Madrid, Spain.
Institute of Investigation 12 de Octubre (i+12), 28041 Madrid, Spain.
Cells. 2021 Nov 1;10(11):2974. doi: 10.3390/cells10112974.
Aging is the result of the deterioration of the homeostatic systems (nervous, endocrine, and immune systems), which preserve the organism's health. We propose that the age-related impairment of these systems is due to the establishment of a chronic oxidative stress situation that leads to low-grade chronic inflammation throughout the immune system's activity. It is known that the immune system weakens with age, which increases morbidity and mortality. In this context, we describe how the function of immune cells can be used as an indicator of the rate of aging of an individual. In addition to this passive role as a marker, we describe how the immune system can work as a driver of aging by amplifying the oxidative-inflammatory stress associated with aging (oxi-inflamm-aging) and inducing senescence in far tissue cells. Further supporting our theory, we discuss how certain lifestyle conditions (such as social environment, nutrition, or exercise) can have an impact on longevity by affecting the oxidative and inflammatory state of immune cells, regulating immunosenescence and its contribution to oxi-inflamm-aging.
衰老是维持机体健康的内稳态系统（神经、内分泌和免疫系统）恶化的结果。我们提出，这些系统与年龄相关的损伤是由于慢性氧化应激状态的建立，导致免疫系统活动中的低水平慢性炎症。众所周知，免疫系统随着年龄的增长而减弱，这会增加发病率和死亡率。在这种情况下，我们描述了如何将免疫细胞的功能用作个体衰老速度的指标。除了作为标志物的这种被动作用外，我们还描述了免疫系统如何通过放大与衰老相关的氧化-炎症应激（氧化-炎症-衰老）以及诱导远隔组织细胞衰老来作为衰老的驱动因素。为了进一步支持我们的理论，我们讨论了某些生活方式条件（如社会环境、营养或运动）如何通过影响免疫细胞的氧化和炎症状态、调节免疫衰老及其对氧化-炎症-衰老的贡献来影响长寿。
