title: Regulatory T cells and IL-10 levels are reduced in patients with vulnerable coronary plaques.
abstract: BACKGROUND
  Despite having a similar large extent of atherosclerotic coronary affliction, some patients suffer of recurrent cardiac events, whereas others remain asymptomatic.
  
  
  OBJECTIVE
  We hypothesized the existence of a systemic "signature" that could distinguish "vulnerable" patients with preexisting coronary atherosclerosis from those having similar risk factors and atheromatous burden, but no history of clinically evident plaque rupture/erosion.
  
  
  METHODS
  Twenty three patients who had at least two prior myocardial infarctions ("vulnerable group") were matched in respect to their background and coronary atherosclerosis extent with twenty one patients without a history of previous myocardial infarction who underwent routine coronary angiography before valvular surgery. We studied a panel of cytokines, antibodies and hormones including IL-6, IL-10, IL-12, antibodies to β2 glycoprotein I (β2GPI), antibodies to oxidized-LDL, adiponectin and resistin, along with levels of circulating EPCs and Tregs.
  
  
  RESULTS
  A significantly higher level of Treg cells was present in the control (73.4%±4) than in the "vulnerable patient" group (62.2%±10.7), p<0.001. IL-10 level was also significantly higher in the control than in the vulnerable patients (2.6±1.2 pg/ml versus 0.9±0.1 pg/ml respectively, p=0.03). There was no significant difference in the circulating levels of the other cytokines, hormones or EPCs between the two groups.
  
  
  CONCLUSIONS
  Regulatory T cells and serum IL-10 may discriminate "vulnerable" versus stable patients and may have a protective role against plaque rupture in patients with coronary atherosclerosis.
authors.affiliation: Heart Institute, Kaplan Medical Center, Rehovot, Affiliated to the Hebrew University and Hadassah Medical School, Jerusalem, Israel. jacobg@post.tau.ac.il
authors.forename: Jacob
authors.initials: J
authors.lastname: George
authors.forename: Shmuel
authors.initials: S
authors.lastname: Schwartzenberg
authors.forename: Diego
authors.initials: D
authors.lastname: Medvedovsky
authors.forename: Michael
authors.initials: M
authors.lastname: Jonas
authors.forename: Gideon
authors.initials: G
authors.lastname: Charach
authors.forename: Arnon
authors.initials: A
authors.lastname: Afek
authors.forename: Ari
authors.initials: A
authors.lastname: Shamiss
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood / Q000150:complications / Q000000981:diagnostic imaging / Q000276:immunology* / Q000473:pathology; D003331:Coronary Vessels / Q000276:immunology* / Q000473:pathology; D018450:Disease Progression; D042783:Endothelial Cells / Q000473:pathology; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D016753:Interleukin-10 / Q000097:blood*; D007557:Israel; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000276:immunology; D058226:Plaque, Atherosclerotic; D012422:Rupture, Spontaneous; D013234:Stem Cells / Q000473:pathology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*
chemical_list: D015415:Biomarkers; C508609:IL10 protein, human; D018836:Inflammation Mediators; D016753:Interleukin-10