Immunosenescence in Human Disease: Mechanistic Insights and Therapeutic Opportunities

Feb 27, 2026Biomolecules & therapeutics

Aging of the Immune System in Human Diseases: How It Happens and Possible Treatments

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Abstract

Immunosenescence is associated with a decline in immune function that may contribute to age-related diseases.

Aging is linked to various changes in the immune system, including loss of naïve T cells and reduced diversity in T cell receptors.
The accumulation of senescent T cells and impaired regulatory T cell function may drive chronic inflammation and tissue damage in autoimmune and metabolic diseases.
In neurodegenerative diseases, aging of microglia and persistent neuroinflammation could worsen neuronal loss.
Immunosenescence may serve as a common mechanism connecting aging with both systemic and organ-specific health issues.
Recent advances in biomarker discovery allow for the quantitative assessment of immune aging.
Emerging therapeutic strategies, such as cytokine modulation and senolytics, could help restore immune function.

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Immunosenescence, an age-associated decline in immune function, is increasingly recognized as a central determinant of health and disease in older adults. Characterized by thymic involution, loss of naïve T cells, contraction of T cell receptor diversity, accumulation of senescent and exhausted lymphocytes, and a chronic inflammatory state known as inflammaging, immunosenescence compromises both innate and adaptive immune responses. Immunosenescence contributes to the pathogenesis of diverse age-related diseases. In autoimmune and metabolic diseases, premature accumulation of senescent T cells and impaired regulatory T cell function drive chronic inflammation and tissue damage, while in neurodegenerative diseases, microglial aging and sustained neuroinflammation exacerbate neuronal loss. These findings highlight immunosenescence as a unifying mechanism linking aging to systemic and organ-specific pathologies. Advances in biomarker discovery, including phenotypic markers, telomere attrition, and epigenetic signatures, have enabled the quantitative assessment of immune aging, while emerging therapeutic strategies, such as cytokine modulation, mTOR inhibition, senolytics, and epigenetic reprogramming, show promise in restoring immune competence. Here, we summarize recent research on immunosenescence in various diseases, particularly chronic inflammatory, metabolic, and neurodegenerative diseases, and suggest novel strategies for the development of senolytic drugs.

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Immunosenescence in Human Disease: Mechanistic Insights and Therapeutic Opportunities

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