Open AccessComparative immunohistochemical and morphometric research of interleukin-17 in various atherosclerotic lesions in human
Author(s) -
Peter V. Pigarevsky,
Пигаревский Петр Валерьевич,
В А Снегова,
Снегова Влада Андреевна,
С.В. Мальцева,
Мальцева Светлана Владимировна,
Natalya G. Davydova,
Давыдова Наталья Геннадиевна
Publication year - 2020
Publication title -
medicinskij akademičeskij žurnal
Language(s) - English
Resource type - Journals
eISSN - 2687-1378
pISSN - 1608-4101
DOI - 10.17816/maj19089
Subject(s) - coronary arteries , pathology , immunohistochemistry , peripheral blood mononuclear cell , autopsy , aorta , fibrous cap , medicine , biology , artery , in vitro , biochemistry
The aim of the artical to investigate cellular and tissue localization of IL-17 in various atherosclerotic lesions of arteries of human and on the basis of the obtained data to make a hypothesis of a possible role of Th17 of cells in destabilization of an atherosclerotic plaque.
Material and methods. On autopsy material by means of histologic, immunohistochemical and morphometric research techniques aorta segments, the coronary arteries and a. basilaris with various types of atherosclerotic lesions (43 samples of tissue) were studied. In samples of tissue studied the endothelial and mononuclear cells expressing IL-17.
Results. It is shown that endothelial cells of an intima are capable to produce IL-17 in all types of atherosclerotic plaques. Increase in number of the mononuclear cells expressing IL-17 in an intima of arteries was at the same time revealed. It is shown that the maximum number of the cells expressing IL-17 was found in an intima of an unstable atherosclerotic plaque, it is especially frequent around a rupture of its cap. What can demonstrate pro-inflammatory action of Th17-cells and IL-17 expressed by them and significant effect them on formation of unstable atherosclerotic lesions.
Conclusion. On the basis of the obtained data for the first time it was succeeded to make a hypothesis of a possible role of Th-17 of cells in destabilization of an atherosclerotic plaque.