Title of article :
CD4⁺Foxp3⁺ Treg and its ICOS⁺ Subsets in Patients with Myocardial Infarction
Author/Authors :
Ghorbani Gazar, Samira Department of Immunology , Andalib, Alireza Department of Immunology , Rezaei, Abbas Department of Immunology , Hashemi, Mohamad Department of Internal Medicine - Isfahan Medical School - Isfahan University of Medical Sciences - Isfahan
Abstract :
Background: Atherosclerosis is a multifactorial disorder with chronic inflammatory
conditions in which immune cells play a significant role in its pathogenic process.
Regulatory T cells (Treg), as a part of immune system, are involved in controlling autoimmune
and inflammatory diseases. Quantitative and/or functional alteration of Tregs
has been shown to play an atheroprotective role and may also promote plaque stabilization.
Objective: To assess if inducible costimulatory molecule (ICOS) expression on
one subtype of Treg cells with high suppressive potential correlates with the pathogenesis
of atherosclerosis. Methods: Patients with myocardial infarction (MI) and/or stable
angina (SA), diagnosed as atherosclerosis by angiography, and a group of individuals
with normal coronary angiography (NCA) were recruited for the present study. Peripheral
blood mononuclear cells (PBMCs) were prepared and the expression of ICOS,
Foxp3 and CD4 molecules was tested by flowcytometry. Results: The percentage of
CD4+Foxp3+ Treg cells was reduced in MI group compared to NCA and SA groups
(p<0.005). Evaluation of the two Treg subsets according to ICOS expression showed a
decreased ICOS+/ICOS- Treg ratio in MI and SA groups compared to NCA individuals
(p=0.002 and p=0.048, respectively). Conclusion: The present data indicate that Tregs
and its ICOS+ subsets are decreased in patients with MI or SA, suggesting a potential
role for Treg in atherosclerosis progression or onset of acute coronary syndrome.
Keywords :
Acute Coronary Syndrome , Stable Angina , Regulatory T Cells , Myocardial Infarction , ICOS , Atherosclerosis , Acute Coronary Syndrome
Journal title :
Astroparticle Physics