DYNAMICS OF THE NK CELL CYTOLYTIC ACTIVITY IN ACUTE MYOCARDIAL INFARCTION: THE ROLE OF CIRCULATING IMMUNE COMPLEXES
DOI:
https://doi.org/10.31082/1728-452X-2020-219-2220-9-10-23-27Keywords:
аcute myocardial infarction, NK cells, circulating immune complexesAbstract
NK cells play an important role in the pathogenesis of atherosclerosis, using their cytotoxic mechanisms that promote the initiation, progression, and rupture of atherosclerotic plaques that leads to acute myocardial infarction. However the data about their cytolytic activity in post-infarction period remain controversial.
The aim of this work was to study the dynamics of changes in the NK cell cytolytic activity within three weeks after acute myocardial infarction in connection with the level of circulating immune complexes in the peripheral blood.
Material and methods. 16 healthy donors and 35 patients after the development of acute myocardial infarction (AMI) on the 1st, 7th and 21st days was studied for the NK cell cytolytic activity of the mononuclear fraction of peripheral blood, evaluated by the cytolysis of erythroleukemia K-562 cells in vitro and levels of serum circulating immune complexes (CIC) using the method of precipitation with polyethylene glycol-6000.
Results and discussion. In the most patients, AMI led to functional anergy of NK cells, but in the smaller part of patients, the increase in their cytotoxicity was observed. The post-infarction period was characterized by an increased content of CIC, the level of which positively correlated with the development of functional anergy of NK cells.
Possible mechanisms for the development of both functional anergy and an increase in NK cell activity in the post-infarction period are discussed.
References
Hansson GK, Hermansson A. The immune system in atherosclerosis. Nat Immunol. 2011;12:204-212. DOI:10.1038/ni.2001
Libby P, Ridker PM, Hansson GK. Progress and challenges in translating the biology of atherosclerosis. Nature. 2011;473:317–325. PMID: 21593864. DOI: 10.1038/nature10146, [Indexed for MEDLINE]
Generali E., Folci M., Selmi C., Riboldi P. Immune-Mediated Heart Disease. In: Sattler S., Kennedy-Lydon T. (eds) The immunology of cardiovascular homeostasis and pathology. Advances in experimental medicine and biology, Vol 1003. Cham: Springer; 2017. P. 145-171. DOI 10.1007/978-3-319-57613-8_8
Yan W, Song Y, Zhou L, et al. Immune cell repertoire and their mediators in patients with acute myocardial infarction or stable angina pectoris. Int J Med Sci. 2017;4(2):181-190. PMID: 28260995, DOI:10.7150/ijms.17119, [Indexed for MEDLINE]
O'Donohoe TJ, Schrale RG, Ketheesan N. The role of anti-myosin antibodies in perpetuating cardiac damage following myocardial infarction. Int J Cardiol. 2016;209:226–233. DOI:10.1016/j.ijcard.2016.02.035
Kaya Z, Leib C, Katus HA. Autoantibodies in heart failure and cardiac dysfunction. Circ Res. 2012;110(1):145-158. DOI: 10.1161/ CIRCRESAHA.111.243360
Рысмендиев А.Ж., Шуратова С.Г., Имантаева Г.М. Иммунология ишемической болезни сердца. - Алматы, 2001. - 109 с. [Rysmendiev AZh, Shuratova SG, Imantaeva GM. Immunologiia ishemicheskoi bolezni serdtsa [I mmunology of ischemic heart disease]. Almaty; 2001. 109 p.]
Lluberas N, Trías N, Brugnini A et al. Lymphocyte subpopulations in myocardial infarction: a comparison between peripheral and intracoronary blood. SpringerPlus. 2015;4(1):744. DOI: 10.1186/ s40064-015-1532-3
Mandal A, Viswanathan Ch. Natural killer cells: In health and disease Hematol Oncol Stem Cell Ther. 2015;8(2):47–55. DOI: http:// dx.doi.org/10.1016/j.hemonc.2014.11.006
Kyaw T, Peter K, Li Y, et al. Cytotoxic lymphocytes and atherosclerosis: significance, mechanisms and therapeutic challenges. British J Pharmacol. 2017;174(22):3956–3972. PMID: 28471481 DOI: 10.1111/bph.13845, [Indexed for MEDLINE]
Bonaccorsi I, De Pasquale C, Campana S, et al. Natural killer cells in the innate immunity network of atherosclerosis. Immunol Lett. 2015;168(1):51-57. DOI: 10.1016/j.imlet.2015.09.006
Yan W, Zhou L, Wen S, et al. Differential loss of natural killer cell activity in patients with acute myocardial infarction and stable angina pectoris. Int J Clin Exp Pathol. 2015;8(11):14667-14675. PMID: 26823790, [Indexed for MEDLINE]
Pedersen BK, Thomsen BS, Nielsen H. Inhibition of natural killer cell activity by antigen-antibody complexes. Allergy. 1986;41:568-574. PMID: 3492939, DOI: 10.1111/j.1398-9995.1986. tb00348.x, [Indexed for MEDLINE]
Magister Š, Tseng HC, Bui VT. Regulation of split anergy in natural killer cells by inhibition of cathepsins C and H and cystatin F. Oncotarget. 2015;8(6):22310-22327. PMID: 26247631, DOI: 10.18632/oncotarget.4208, [Indexed for MEDLINE]
Abdul-Hassan A, Al-Hassan A. Cytokines profile in patients with acute myocardial infarction. J Al-Nahrain Univers Science. 2012;15(4):161-167. PMID: 28683166. DOI: 10.1111/eci.12785. [Indexed for MEDLINE]
Saadoun D, Rosenzwajg M, Joly F, et al. Regulatory T-cell responses to low-dose interleukin-2 in HCV-induced vasculitis. N Engl J Med. 2011;365:2067–2077. DOI: 10.1056/NEJMoa1105143
Zhao TX, Kostapanos M, Griffiths Ch, et al. Low-dose interleukin-2 in patients with stable ischaemic heart disease and acute coronary syndromes (LILACS): protocol and study rationale for a randomised, double-blind, placebo-controlled, phase I/II clinical trial. BMJ Open. 2018;8:e022452. PMID: 30224390, DOI: 10.1136/ bmjopen-2018-022452, [Indexed for MEDLINE]
