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Hedi Raizer

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How does immunosenescence work?

Immunosenescence is the age-related decline in immune function, driven by thymic involution, chronic low-grade inflammation, and the accumulation of senescent immune cells. This page outlines the mechanisms and the resea

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How does immunosenescence work?

Immunosenescence is the formal term for the progressive deterioration of the immune system associated with aging. It is not a single entity but a collection of changes across innate and adaptive immunity, including telomere shortening, chronic low-grade inflammation, thymic dysfunction, and the expansion of senescent immune cell subsets [1]. These alterations are observed in physiological aging and are also a feature of autoimmune conditions such as systemic lupus erythematosus (SLE), where they appear early and contribute to disease activity and organ damage [1].

The work centres on the thymus and its output, particularly the peptide hormone thymosin alpha-1 (Tα1), which is produced by the thymus and exhibits immunomodulatory, anti-inflammatory, and antioxidant properties [2].

Research Studies

Thymosin alpha-1 and thymic output in aging

Thymic involution—the age-related shrinkage of the thymus—leads to reduced T-cell production, chronic inflammation, and increased susceptibility to age-related diseases [2]. Tα1 stimulates T-cell differentiation, enhances thymic output, and modulates dendritic cell and macrophage activity [2]. Preclinical and clinical studies show that Tα1 can improve vaccine response in the elderly and mitigate immunosenescence [2].

Thymosin alpha-1 and immunosenescence in early-stage NSCLC

A clinical trial is exploring the effect of Tα1 on postoperative peripheral blood circulating tumor cells and immunosenescence in patients with early-stage non-small cell lung cancer (NSCLC) [4]. This study focuses on a specific cancer population and surgical context.

Nicotinamide mononucleotide and immunosenescence in metabolic disorders

A placebo-controlled clinical trial investigated the effect of nicotinamide mononucleotide (NMN) supplementation on immunosenescence in middle-aged and elderly individuals with metabolic disorders [3]. The study also assessed glucose and lipid metabolism, aiming to provide a new method to improve immunosenescence [3].

Alpha-ketoglutarate and surgical stress in older patients

Coronary artery bypass grafting (CABG) is performed in approximately 400,000 patients in the United States each year and invokes a massive surgical stress response, with systemic epinephrine increasing 33-fold and norepinephrine increasing 3-fold [5]. This response involves sterile inflammation, damage-associated molecular patterns (DAMPs), and activation of neutrophils, leading to a cascade of cytokines, complement, and coagulation changes [5]. A trial is investigating alpha-ketoglutarate for geroprotection in this context [5].

Taxifolin/ergothioneine and immune biomarkers in healthy volunteers

Immune function declines with age, resulting in impaired vaccination responses and increased risk of infections and severe complications [6]. A study is examining the impact of taxifolin/ergothioneine on immune biomarkers in healthy volunteers, acknowledging the challenge of measuring dietary interventions on immune function [6].

Nicotinamide adenine dinucleotide and immunosenescence in menopause

Menopause is associated with progressive estrogen depletion and increased susceptibility to age-associated disorders, involving mechanisms such as mitochondrial dysfunction, oxidative stress, chronic inflammation, genomic instability, and immunosenescence [7].

Bone immunity and immunosenescence in bone metabolism

Bone metabolism is regulated by immune cells that maintain skeletal homeostasis through cytokine secretion and cell interactions; disruption by inflammation, autoimmunity, or aging drives pathological bone diseases including osteoporosis and rheumatoid arthritis [8].

NMN co-treatment with hUC-MSCs in aging models

Human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) are a promising therapeutic option for anti-ageing therapy, but the ageing microenvironment can induce oxidative stress and senescence in transplanted hUC-MSCs, impairing their capacity to delay immunosenescence [9]. Combining MSC-based approaches with NMN is under investigation in D-galactose-induced ageing mice and cellular senescence models [9].

Irisin and the aging immune landscape in sepsis

Irisin, a muscle-secreted myokine induced by exercise, serves as a molecular bridge between muscle activity and the immune system; in aging, it may modulate the transition toward immunosenescence and influence host vulnerability to acute systemic inflammation [10].

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