Features of cellular immunity in patients with CHD complicated by metabolic syndrome
DOI:
https://doi.org/10.11603/bmbr.2706-6290.2022.2.13042Keywords:
lymphocyte subpopulations, metabolic syndrome, coronary heart diseaseAbstract
Summary. The article presents changes in cellular immunity in patients with coronary heart disease complicated by metabolic syndrome (MS). Coronary heart disease (CHD) is the most common form of heart disease. The main trigger in the development of CVD are inflammatory processes and metabolic syndrome, accompanied by the development of immunodeficiency.
The aim of the study – to research the state of cellular immunity in patients with coronary heart disease on the background of metabolic syndrome.
Materials and Methods. 120 patients with verified coronary heart disease were examined, including 60 patients with coronary heart disease without MS – group 1 (30 men, 30 women) and 60 patients with coronary heart disease on the background of MS – group 2 (29 men, 31 women). The mean age of patients was (50±5) years. Control group – 30 healthy people of appropriate age and sex.
Results. In patients with coronary heart disease there was a decrease in the absolute number of T-lymphocytes (CD3 +), a subpopulation of T-helpers (CD 4+) and the absolute number of T- effectors (CD8 +) exceeded the control group. The content of activated T-lymphocytes (CD 25+) was 2.9 times higher than normal. In the group of patients with coronary heart disease complicated by metabolic syndrome, the content of the absolute number of T-lymphocytes was within normal limits. The level of T-helpers was 54 % lower than normal and 24 % higher than in group 1. The content of T-effectors in patients from this group was 65 % higher than normal. The level of activated T-lymphocytes in patients from the second group exceeded the control rate by 2.8 times. In patients of both groups, activation of B-cell and killer immune systems is observed. Changes in the levels of T-lymphocyte subpopulations in the examined both groups indicate the presence of T-cell immunodeficiency. The level of activated T-killers (CD 25+) is increased in both groups.
Conclusions. Activated humoral and killer immunity on the background of deficiency of T-cell immunity in the examined patients indicates the presence of dysfunction of the immune system, which is a pathogenetic link in the development of cardiovascular pathology. Complications of coronary heart disease with metabolic syndrome revealed an increased level of effectors, which also have a supresor function, which causes more severe immunodeficiency.
References
Thorkelsdottir T, Johannesdottir H, Arnadottir LO, Adalsteinsson J, Gardarsdottir HR, Helgason D, et al. No significant association between obesity and long-term outcome of coronary artery bypass grafting. Laeknabladid. 2019;105(7): 319-26. DOI: 10.17992/lbl.2019.0708.240.
Metabolic Syndrome [Internet] / National Library of Medicine. StatPearls. 2022. Available from: https://pubmed.ncbi.nlm.nih.gov/29083742/
Phoksawat W, Jumnainsong A, Leelayuwat N, Leelayuwat C. IL-17 production by NKG2D-expressing CD56+ T cells in type 2 diabetes. Molecular Immunology. 2019;106: 22-8.
Lapovets LIe, Akimova VM, Lebid HB, Martianova OI, Polovkovych SV. Laboratiry immunology guide. [Посібник з лабораторної імунології] Lviv. Vydavets Marchenko T.V.; 2021. Ukrainian.
Bantug GR, Galluzzi L, Kroemer G, Hess C. The spectrum of T cell metabolism in health and disease. Nature Reviews Immunology. 2018;18(1): 19-34. DOI: 10.1038/nri.2017.99.
Mauss D, Herr RM, Jarczok MN, Motoc I, Fischer JE, Bosch JA. The association of cortisol levels with leukocyte distribution is disrupted in the metabolic syndrome. Obesity Research & Clinical Practic. 2021;15(1): 78-84. DOI: 10.1016/j.orcp.2020.12.003.
Roos CJ, Quax PH, Jukema JW. Cardiovascular metabolic syndrome: mediators involved in the pathophysiology from obesity to coronary heart disease. Biomark Med. 2012;6(1): 35-52. DOI: 10.2217/bmm.11.105. PMID: 22296195.
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