IL-17 producing CD4+CD45RO+ T-cells in atherosclerosis express GITR molecule
Background: Atherosclerosis (AS) is a chronic inflammatory disease of vessel walls associated with infiltration of immune cells which their function is controlled by different co-stimulatory and co-inhibitory receptors. We investigated the expression of co-inhibitory molecules on the memory and effe...
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BMC
2017-12-01
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Series: | Artery Research |
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Online Access: | https://www.atlantis-press.com/article/125924954/view |
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author | Atefe Ghamar Talepoor Negar Behnamfar Mohammad Javad Zibaeenezhad Mehrnoosh Doroudchi |
author_facet | Atefe Ghamar Talepoor Negar Behnamfar Mohammad Javad Zibaeenezhad Mehrnoosh Doroudchi |
author_sort | Atefe Ghamar Talepoor |
collection | DOAJ |
description | Background: Atherosclerosis (AS) is a chronic inflammatory disease of vessel walls associated with infiltration of immune cells which their function is controlled by different co-stimulatory and co-inhibitory receptors. We investigated the expression of co-inhibitory molecules on the memory and effector T-cells in patients with Atherosclerosis.
Methods: Patients included 9 hypertensive, dyslipidemic, non-diabetic, non-smoker individuals with the diagnosis of coronary artery disease and controls were 8 normotensive, normolipemic, non-diabetic, non-smoker individuals with normal coronary angiography/insignificant coronary artery disease. PBMCs were separated from the blood and memory T-cell subsets as well as the expression of Glucocorticoid-induced tumor necrosis factor receptor (GITR), Programmed Death-1 (PD-1), IL-17A and IFN-γ were quantified by flowcytometry.
Results: CD4+CD45RO+ memory T-cells and CD4+CD45RO− effector T-cells in patients expressed the highest level of GITR molecule. The IL-17 producing memory CD4+CD45RO+ T-cells were enriched in GITR molecule in the patients group (P = 0.03). The increased population of GITR+effector CD4+CD45RO− T-cells in patients, however, did not produce IL-17 (P = 0.03). PD-1 expression on memory T-cells of the patients was higher than the controls and was concomitant with the lack of IFN-γ expression (P = 0.05). IFN-γ production by effector T-cells was only seen in the PD-1− population in both groups.
Conclusions: We provide data on the expression of GITR molecule on IL-17 producing memory T-cells in patients with CAD. A population of memory T-cells, which expressed PD-1 and were not producing IFN-γ, also increased in patients’ blood. These data suggest the modified phenotype/function of T-cell subsets in the atherosclerotic inflammation. |
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issn | 1876-4401 |
language | English |
last_indexed | 2024-04-14T05:24:34Z |
publishDate | 2017-12-01 |
publisher | BMC |
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series | Artery Research |
spelling | doaj.art-9a2fa9acd0a148208bf59c62ee156d762022-12-22T02:10:03ZengBMCArtery Research1876-44012017-12-012110.1016/j.artres.2017.12.004IL-17 producing CD4+CD45RO+ T-cells in atherosclerosis express GITR moleculeAtefe Ghamar TalepoorNegar BehnamfarMohammad Javad ZibaeenezhadMehrnoosh DoroudchiBackground: Atherosclerosis (AS) is a chronic inflammatory disease of vessel walls associated with infiltration of immune cells which their function is controlled by different co-stimulatory and co-inhibitory receptors. We investigated the expression of co-inhibitory molecules on the memory and effector T-cells in patients with Atherosclerosis. Methods: Patients included 9 hypertensive, dyslipidemic, non-diabetic, non-smoker individuals with the diagnosis of coronary artery disease and controls were 8 normotensive, normolipemic, non-diabetic, non-smoker individuals with normal coronary angiography/insignificant coronary artery disease. PBMCs were separated from the blood and memory T-cell subsets as well as the expression of Glucocorticoid-induced tumor necrosis factor receptor (GITR), Programmed Death-1 (PD-1), IL-17A and IFN-γ were quantified by flowcytometry. Results: CD4+CD45RO+ memory T-cells and CD4+CD45RO− effector T-cells in patients expressed the highest level of GITR molecule. The IL-17 producing memory CD4+CD45RO+ T-cells were enriched in GITR molecule in the patients group (P = 0.03). The increased population of GITR+effector CD4+CD45RO− T-cells in patients, however, did not produce IL-17 (P = 0.03). PD-1 expression on memory T-cells of the patients was higher than the controls and was concomitant with the lack of IFN-γ expression (P = 0.05). IFN-γ production by effector T-cells was only seen in the PD-1− population in both groups. Conclusions: We provide data on the expression of GITR molecule on IL-17 producing memory T-cells in patients with CAD. A population of memory T-cells, which expressed PD-1 and were not producing IFN-γ, also increased in patients’ blood. These data suggest the modified phenotype/function of T-cell subsets in the atherosclerotic inflammation.https://www.atlantis-press.com/article/125924954/viewAtherosclerosisImmunopathologyT cellInflammation |
spellingShingle | Atefe Ghamar Talepoor Negar Behnamfar Mohammad Javad Zibaeenezhad Mehrnoosh Doroudchi IL-17 producing CD4+CD45RO+ T-cells in atherosclerosis express GITR molecule Artery Research Atherosclerosis Immunopathology T cell Inflammation |
title | IL-17 producing CD4+CD45RO+ T-cells in atherosclerosis express GITR molecule |
title_full | IL-17 producing CD4+CD45RO+ T-cells in atherosclerosis express GITR molecule |
title_fullStr | IL-17 producing CD4+CD45RO+ T-cells in atherosclerosis express GITR molecule |
title_full_unstemmed | IL-17 producing CD4+CD45RO+ T-cells in atherosclerosis express GITR molecule |
title_short | IL-17 producing CD4+CD45RO+ T-cells in atherosclerosis express GITR molecule |
title_sort | il 17 producing cd4 cd45ro t cells in atherosclerosis express gitr molecule |
topic | Atherosclerosis Immunopathology T cell Inflammation |
url | https://www.atlantis-press.com/article/125924954/view |
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