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Review
. 2022 Apr 27:3:840827.
doi: 10.3389/fragi.2022.840827. eCollection 2022.

Inflammation, Immune Senescence, and Dysregulated Immune Regulation in the Elderly

Carey Shive  1   2 , Pushpa Pandiyan  2
Affiliations
Review

Inflammation, Immune Senescence, and Dysregulated Immune Regulation in the Elderly

Carey Shive et al. Front Aging. .

Abstract

An optimal immune response requires the appropriate interaction between the innate and the adaptive arms of the immune system as well as a proper balance of activation and regulation. After decades of life, the aging immune system is continuously exposed to immune stressors and inflammatory assaults that lead to immune senescence. In this review, we will discuss inflammaging in the elderly, specifically concentrating on IL-6 and IL-1b in the context of T lymphocytes, and how inflammation is related to mortality and morbidities, specifically cardiovascular disease and cancer. Although a number of studies suggests that the anti-inflammatory cytokine TGF-b is elevated in the elderly, heightened inflammation persists. Thus, the regulation of the immune response and the ability to return the immune system to homeostasis is also important. Therefore, we will discuss cellular alterations in aging, concentrating on senescent T cells and CD4+ CD25+ FOXP3+ regulatory T cells (Tregs) in aging.

Keywords: dysregulated tregs; elderly; immune senescence; inflammaging; inflammation; t cell senescence.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
Model. Persistent elevation of innate cytokines such as IL-6, IL-1β, TNFα, and TGF-β, contribute to immunosenescence in the elderly. These cytokines also promote T cell senescence. Senescent T cells perpetuate inflammation by secreting inflammatory cytokines. IL-6 also may promote the development of dysfunctional regulatory T cells (TregDys), indirectly contributing to chronic inflammation in the elderly. The result is aging and immune and non-immune diseases of aging.
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