title: Expansion of myeloid-derived suppressor cells in patients with acute coronary syndrome.
abstract: OBJECTIVE
  The aim of this study was to explore whether the circulating frequency and function of myeloid-derived suppressor cells (MDSCs) are altered in patients with acute coronary syndrome (ACS).
  
  
  METHODS
  The frequency of MDSCs in peripheral blood was determined by flow cytometry, and mRNA expression in purified MDSCs was analyzed by real-time reverse transcription polymerase chain reaction (RT-PCR). The suppressive function of MDSCs isolated from different groups was also determined. The plasma levels of certain cytokines were determined using Bio-Plex Pro™ Human Cytokine Assays.
  
  
  RESULTS
  The frequency of circulating CD14(+)HLA-DR(-/low) MDSCs; arginase-1 (Arg-1) expression; and plasma levels of interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and IL-33 were markedly increased in ACS patients compared to stable angina (SA) or control patients. Furthermore, MDSCs from ACS patients were more potent suppressors of T-cell proliferation and IFN-γ production than those from the SA or control groups at ratios of 1:4 and 1:2; this effect was partially mediated by Arg-1. In addition, the frequency of MDSCs was positively correlated with plasma levels of IL-6, IL-33, and TNF-α.
  
  
  CONCLUSIONS
  We observed an increased frequency and suppressive function of MDSCs in ACS patients, a result that may provide insights into the mechanisms involved in ACS.
authors.affiliation: Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
authors.forename: Yan-ge
authors.initials: YG
authors.lastname: Wang
authors.forename: Xin
authors.initials: X
authors.lastname: Xiong
authors.forename: Zhu-yue
authors.initials: ZY
authors.lastname: Chen
authors.forename: Kan-ling
authors.initials: KL
authors.lastname: Liu
authors.forename: Jin-hua
authors.initials: JH
authors.lastname: Yang
authors.forename: Qiang
authors.initials: Q
authors.lastname: Wen
authors.forename: Fang-qin
authors.initials: FQ
authors.lastname: Wu
authors.forename: Xiao-fan
authors.initials: XF
authors.lastname: Hu
authors.forename: Yu-dong
authors.initials: YD
authors.lastname: Peng
authors.forename: Jing-jing
authors.initials: JJ
authors.lastname: Wu
authors.forename: Yi-tian
authors.initials: YT
authors.lastname: Lian
authors.forename: Wen-cai
authors.initials: WC
authors.lastname: Zhang
authors.forename: Long-xian
authors.initials: LX
authors.lastname: Cheng
mesh_terms: D054058:Acute Coronary Syndrome / Q000378:metabolism / Q000473:pathology*; D060050:Angina, Stable / Q000378:metabolism / Q000473:pathology; D001119:Arginase / Q000235:genetics / Q000378:metabolism; D049109:Cell Proliferation; D002478:Cells, Cultured; D004562:Electrocardiography; D005260:Female; D006684:HLA-DR Antigens / Q000378:metabolism; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D053583:Interleukin-1beta / Q000097:blood; D000067596:Interleukin-33; D015850:Interleukin-6 / Q000097:blood; D007378:Interleukins / Q000097:blood; D007963:Leukocytes, Mononuclear / Q000166:cytology; D018950:Lipopolysaccharide Receptors / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D022423:Myeloid Cells / Q000166:cytology / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D013601:T-Lymphocytes / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D006684:HLA-DR Antigens; C506536:IL33 protein, human; D053583:Interleukin-1beta; D000067596:Interleukin-33; D015850:Interleukin-6; D007378:Interleukins; D018950:Lipopolysaccharide Receptors; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma; C574619:ARG1 protein, human; D001119:Arginase