Cellular and humoral mechanisms of immune aging

Despite significant advancements in extending average life expectancy, challenges persist in enhancing the quality of life for elderly and senile individuals, preventing and treating age-associated diseases and managing geriatric syndromes. The immune system plays a crucial role in aging, undergoing extensive functional changes collectively referred to as immunosenescence. Cellular aging within the immune system is associated with telomere shortening, proteostasis loss, mitochondrial dysfunction, DNA damage, and oxidative stress. Senescent cells are characterized by resistance to apoptosis, cell cycle arrest, and abnormal production of pro-inflammatory cytokines, leading to chronic low-grade inflammation. Concurrently, the effector mechanisms of the immune response become depleted, resulting in a reduced ability of the immune system to adequately respond to antigenic stimuli. Thymic atrophy, depletion of bone marrow niches, a shift in hematopoiesis toward the myeloid lineage, and alterations in lymphocyte subpopulation ratios occur. Additionally, the effector functions of neutrophil granulocytes are impaired. However, the nature of these functional changes in immunosenescence remains insufficiently studied, requiring further research to determine the specific dysfunctions of neutrophil granulocytes in aging.