title: CD4⁺Foxp3⁺ Treg and its ICOS⁺ subsets in patients with myocardial infarction.
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 auto-immune and inflammatory diseases. Tregs have 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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Immunology, Isfahan Medical School, Isfahan University of Medical Sciences, Isfahan, Iran, e-mail: Andalib@med.mui.ac.ir.
authors.forename: Samira
authors.initials: S
authors.lastname: Ghourbani Gazar
authors.forename: Alireza
authors.initials: A
authors.lastname: Andalib
authors.forename: Mohamad
authors.initials: M
authors.lastname: Hashemi
authors.forename: Abbas
authors.initials: A
authors.lastname: Rezaei
mesh_terms: D000328:Adult; D000368:Aged; D060050:Angina, Stable / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D002478:Cells, Cultured; D005260:Female; D005434:Flow Cytometry; D051858:Forkhead Transcription Factors / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D060889:Inducible T-Cell Co-Stimulator Protein / Q000276:immunology* / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000378:metabolism; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000378:metabolism
chemical_list: C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; C556692:ICOS protein, human; D060889:Inducible T-Cell Co-Stimulator Protein