title: Upregulation of OX40-OX40 ligand system on T lymphocytes in patients with acute coronary syndromes.
abstract: OBJECTIVE
  To investigate whether upregulation of OX40-OX40 ligand (OX40L) system is related to stability of coronary atherosclerotic plaque in patients with coronary heart diseases.
  
  
  METHODS
  Thirty normal controls and 250 patients, including 80 with stable angina (SA), 110 with unstable angina (UA), and 60 with acute myocardial infarction (AMI), were enrolled in our study. The expression of OX40 and OX40L in peripheral CD4 T lymphocytes were analyzed by flow cytometry. Serum soluble OX40L (sOX40L) and C-reactive protein levels were measured by commercially available enzyme-linked immunosorbent assay kit.
  
  
  RESULTS
  The expression of OX40 and OX40L in peripheral CD4 T lymphocytes in patients with UA [26.7 +/- 3.4 and 45.5 +/- 8.1 mean fluorescence intensity (MFI)] and AMI (27.4 +/- 4.6 and 55.7 +/- 9.4 MFI) were significantly higher than those in patients with SA (6.5 +/- 1.4 and 12.4 +/- 3.2 MFI) and controls (7.3 +/- 1.5 and 11.9 +/- 6.1 MFI). sOX40L in patients with UA (38.7 +/- 6.9 ng/mL) and AMI (39.5 +/- 7.3 ng/mL) were significantly higher than those in patients with SA (8.4 +/- 1.4 ng/mL) (P < 0.01) and controls (8.9 +/- 2.3 ng/mL) (P < 0.01). C-reactive protein level in serum in patients with UA (14.6 +/- 3.3 ng/mL) and AMI (15.0 +/- 4.3 ng/mL) were also higher than those in patients with SA (1.4 +/- 0.4 ng/mL) and controls (1.3 +/- 0.3 ng/mL). It was interesting that there was a peak level of sOX40L at 12 hours after AMI in patients with AMI. A positive correlation was found between sOX40L and serum C-reactive protein levels (r = 0.71; P < 0.0001).
  
  
  CONCLUSIONS
  Patients with acute coronary syndromes showed increased coexpression of OX40 system, which may create a proinflammatory and prothrombotic milieu for aggravating the development of atherosclerosis and instability of atherosclerotic plaques, and sOX40L is a potential marker for predicting the severity of coronary heart diseases.
authors.affiliation: Department of Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, China. yanjinchuan@hotmail.com
authors.forename: JinChuan
authors.initials: J
authors.lastname: Yan
authors.forename: Guanghua
authors.initials: G
authors.lastname: Chen
authors.forename: Jie
authors.initials: J
authors.lastname: Gong
authors.forename: CuiPing
authors.initials: C
authors.lastname: Wang
authors.forename: Rongzeng
authors.initials: R
authors.lastname: Du
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood* / Q000378:metabolism; D000368:Aged; D000789:Angina, Unstable / Q000097:blood / Q000378:metabolism; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism*; D016022:Case-Control Studies; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000378:metabolism; D053278:OX40 Ligand / Q000096:biosynthesis* / Q000097:blood; D011237:Predictive Value of Tests; D015854:Up-Regulation
chemical_list: D015415:Biomarkers; D053278:OX40 Ligand; C089251:TNFSF4 protein, human; D002097:C-Reactive Protein