IL-17 producing CD4+CD45RO+ T-cells in atherosclerosis express GITR molecule

Abstract

BackgroundAtherosclerosis (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. MethodsPatients 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. ResultsCD4+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. ConclusionsWe 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.