title: Lower prevalence of circulating natural killer T cells in patients with angina: a potential novel marker for coronary artery disease.
abstract: OBJECTIVE
  Atherosclerosis is an inflammatory disease. Natural killer T cells are a unique lymphocyte subset that can recognize lipid antigens presented by CD1d and secrete copious amounts of pro-atherogenic cytokines such as interferon-gamma. We have previously shown that natural killer T cells accelerate atherosclerosis in mice and macrophages incubated with oxidized low-density lipoproteins induce natural killer T cells to produce interferon-gamma. Thus, whether the prevalence of natural killer T cells in peripheral blood is altered in patients with angina pectoris and its correlation with coronary risk factors was determined.
  
  
  METHODS
  Cell profiling was performed using flow cytometry in patients with stable angina, unstable angina (Braunwald IIIB), and healthy controls. Natural killer T cells in peripheral blood were identified by the expression of natural killer T specific invariant T cell receptor alpha-chain (Valpha24) and T cell receptor beta-chain (Vbeta11).
  
  
  RESULTS
  Prevalence of natural killer T (Valpha24-Vbeta11 double positive) cells was significantly decreased in patients with unstable angina and stable angina compared with that in controls. No significant differences were observed in the prevalence between unstable and stable angina. Reduction of natural killer T cells was independently associated with the presence of angina.
  
  
  CONCLUSIONS
  Lower prevalence of circulating natural killer T cells is related to the presence of coronary artery disease. As T cell receptor down-regulation or apoptosis after natural killer T cell activation and subsequent interferon-gamma release may contribute to atherogenesis, natural killer T cells can become a novel therapeutic target for the prevention and treatment of atherosclerotic vascular diseases.
authors.affiliation: Department of Cardiovascular Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Andoh
authors.forename: Satoshi
authors.initials: S
authors.lastname: Fujii
authors.forename: Kazuya
authors.initials: K
authors.lastname: Iwabuchi
authors.forename: Takashi
authors.initials: T
authors.lastname: Yokota
authors.forename: Naoki
authors.initials: N
authors.lastname: Inoue
authors.forename: Yukihito
authors.initials: Y
authors.lastname: Nakai
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Mishima
authors.forename: Takehiro
authors.initials: T
authors.lastname: Yamashita
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Nakagawa
authors.forename: Akira
authors.initials: A
authors.lastname: Kitabatake
authors.forename: Kazunori
authors.initials: K
authors.lastname: Onoe
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Tsutsui
mesh_terms: D000787:Angina Pectoris / Q000276:immunology*; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D003324:Coronary Artery Disease / Q000276:immunology*; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D015995:Prevalence