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Adaptive immunity plays a profound role in atherosclerosis pathogenesis by regulating antigen-specific responses, inflammatory signaling and antibody production. However, as we age, our immune system undergoes a gradual functional decline, a phenomenon termed “immunosenescence”. This decline is characterized by a reduction in proliferative naïve B- and T cells, decreased B- and T cell receptor repertoire and a pro-inflammatory senescence associated secretory profile. Furthermore, aging affects germinal center responses and deteriorates secondary lymphoid organ function and structure, leading to impaired T-B cell dynamics and increased autoantibody production. In this review, we will dissect the impact of aging on adaptive immunity and the role played by age-associated B- and T cells in atherosclerosis pathogenesis, emphasizing the need for interventions that target age-related immune dysfunction to reduce cardiovascular disease risk.
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Roy P. M. Snijckers
Amanda C. Foks
Frontiers in Immunology
Leiden University
Centre for Human Drug Research
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Snijckers et al. (Mon,) studied this question.
www.synapsesocial.com/papers/68e6f047b6db64358766adc0 — DOI: https://doi.org/10.3389/fimmu.2024.1350471