TY - JOUR
T1 - Lower prevalence of circulating natural killer T cells in patients with angina
T2 - A potential novel marker for coronary artery disease
AU - Andoh, Yasuhiro
AU - Fujii, Satoshi
AU - Iwabuchi, Kazuya
AU - Yokota, Takashi
AU - Inoue, Naoki
AU - Nakai, Yukihito
AU - Mishima, Tetsuya
AU - Yamashita, Takehiro
AU - Nakagawa, Toshiaki
AU - Kitabatake, Akira
AU - Onoe, Kazunori
AU - Tsutsui, Hiroyuki
N1 - Copyright:
Copyright 2011 Elsevier B.V., All rights reserved.
PY - 2006/9
Y1 - 2006/9
N2 - 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-γ. 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-γ. 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. METHOD: 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 α-chain (Vα24) and T cell receptor β-chain (Vβ11). RESULTS: Prevalence of natural killer T (Vα24-Vβ11 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-γ release may contribute to atherogenesis, natural killer T cells can become a novel therapeutic target for the prevention and treatment of atherosclerotic vascular diseases.
AB - 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-γ. 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-γ. 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. METHOD: 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 α-chain (Vα24) and T cell receptor β-chain (Vβ11). RESULTS: Prevalence of natural killer T (Vα24-Vβ11 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-γ release may contribute to atherogenesis, natural killer T cells can become a novel therapeutic target for the prevention and treatment of atherosclerotic vascular diseases.
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U2 - 10.1097/00019501-200609000-00005
DO - 10.1097/00019501-200609000-00005
M3 - Article
C2 - 16905964
AN - SCOPUS:33747157659
SN - 0954-6928
VL - 17
SP - 523
EP - 528
JO - Coronary Artery Disease
JF - Coronary Artery Disease
IS - 6
ER -