Immunosenescence and Clinical Consequences

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Background

The decrease in death rates generated increased longevity in most countries around the world. However, a similar increase in disability-free life expectancy has not been reached and thus people living long-term will likely develop one or more chronic diseases (multimorbidity). Hypertension, diabetes, obesity, sarcopenia, Alzheimer's, cancer, chronic obstructive pulmonary diseases, poor responses to infection and vaccination are examples of common isolated or associated conditions of old individuals. In addition, most age-related diseases have been associated with chronic inflammatory processes (inflammageing) and/or decline in immune function (immunosenescence).

Immunosenescence is characterized by changes in innate and adaptive branches of the immune system. Altered hematopoiesis (decrease in lymphoid and increase in myeloid cells percentages) and changes in thymic structure/function are in part responsible for the diminished presence of naïve B and T lymphocytes in the periphery. Accumulation of myeloid-derived suppressor cells and late differentiated T cells is also observed. The reduction in the secreted IL-2 and proliferative capacity of T cells are compensated by homeostatic proliferation driven by IL-7 and IL-15. These changes have been associated with poor immune responses to infections and vaccination, cancer progression, leading to repeated hospitalizations and death. Moreover, the most important cells from the innate arm of the immune system are also affected. Neutrophils migration to inflammatory sites, activity as a phagocyte, and neutrophil extracellular traps impairment have been reported. Monocytes present changes in TLR (toll-like receptors) expression leading to either decrease or increase in cytokines secretion. These modifications are responsible at least in part for the reduced efficacy in the clearing of pathogens, wound healing, and resolution of inflammation. The increased secretion of pro-inflammatory mediators (cytokines, acute phase proteins) and reduced levels of anti-inflammatory factors have been correlated with a low grade of chronic inflammation (inflammageing) that possibly impact age-related diseases.

To reduce the burden of disease, a pathway of effective prevention to diminish risk factors is the best alternative. Using cardiovascular disease as an example, preventive programs should take into account blood pressure, body-mass index, fasting glucose, cholesterol, diet, and physical activity. Associations between sedentary individuals and poor response to vaccines or physical activity and reduction in all-cause mortality have emerged. These results suggest that immune responses can be modulated by healthy habits such as physical activity, adequate diet, in detriment of unhealthy habits as sedentary, tobacco and alcoholism.

The understanding of how the immune system changes with age and can potentially be modulated will add knowledge of how older individuals can reach healthspan and also direct public policy actions in order to provide adequate care for those individuals in ill health.

The aim of this Research Topic is to gather knowledge of how immunosenescence can be targeted for clinical use. We welcome authors to submit Original Research, Reviews, Mini-Review, Hypothesis&Theory, Clinical Trials, Case Reports, and Opinions focusing on the following subtopics:

1. Cellular and molecular aspects of Immunosenescence
2. Immunosenescence and age-related diseases
3. Infection/vaccination and Immunosenescence
4. Immunosenescence, cancer and check point therapies
5. Frailty and immunosenescence

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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