Introduction. Cellular aging is described as the irreversible loss of the ability of cells to pro-liferate, caused by stressful effects. The accumulation of aging cells has been described in various inflammatory diseases and can be both a consequence of inflammation and contribute to its maintenance, which is due to increased production of proinflammatory cytokines by aging cells. Aim – to conduct a quantitative and qualitative assessment of senescent subpopulations of blood mononuclear cells (MNCs) in patients with a chronic inflammatory skin disease – atopic dermatitis. Material and methods. Blood MNCs were isolated from heparinized venous blood of patients and healthy donors in a Ficoll density gradient. To identify senescent cells, MNCs were stained with conjugates of antibodies to surface markers (CD3, CD56, CD14, CD19) and to intracellular proteins – markers of cellular senescence (p21WAF1/CIP1, p16INK4A ), after which they were analyzed by flow cytometry. Senescence-associated beta-galactosidase activity was measured by flow cytometry after incubation of cells with a specific fluorogenic substrate. Plasma IL-6 levels were measured using ELISA. Results. Senescent cells with p21+p16+ phenotype were detected in all studied subpopula-tions of peripheral blood MNCs in both healthy donors and patients. Significantly higher num-ber of senescent cells was found in CD3+CD56+-T-cell subpopulation in patients compared to healthy donors. Senescence-associated beta-galactosidase activity in monocyte, T cell, and NK cell subsets in patients correlated with disease severity. Moderate positive correlation of plasma IL-6 levels with age was found in the atopic dermatitis group, which was absent in the healthy donor group. Conclusion. For the first time was performed quantitative evaluation of senescent cells among blood MNCs in patients with atopic dermatitis. Increased content of senescent cells for patients compared to healthy donors was revealed in CD3+CD56+-T-cell subpopulation. © 2025 Elsevier B.V., All rights reserved.