title: Inhibition of IFN regulatory factor-1 down-regulate Th1 cell function in patients with acute coronary syndrome.
abstract: BACKGROUND
  The crucial role of T helper (Th) cells and chronic inflammation in atherosclerosis and coronary artery disease is no longer controversial. Evidence has revealed that Th cell type 1 (Th1) is closely associated with the pathogenesis of acute coronary syndrome (ACS). But the mechanisms involved in the generation of Th1 cells have not been fully elucidated. IFN regulatory factor (IRF)-1 is a pleiotropic transcription factor involved in innate immunity and chronic inflammation disease. The study was undertaken to investigate the potential effect of IRF-1 on the Th1 cell function in patients with ACS in vitro.
  
  
  METHODS
  Patients with clinical presentation of chest pain, stable angina, unstable angina, and acute myocardial infarction were enrolled in this study. Circulating CD4+ T cells were enriched and analyzed for mRNA and protein expression of IRF-1. Silencing IRF-1 gene with small interfering RNA in CD4+ T cells from patients with ACS was performed to explore the possible mechanisms involved in ACS.
  
  
  RESULTS
  The results demonstrated that the expression of IRF-1 in CD4+ T cells was significantly increased in patients with ACS and positively correlated with plasma Th1 cytokine profile. Inhibition of IRF-1 in CD4+ T cells from patients with ACS prevented the induction of the frequencies and cytokines expression of Th1 cells. In addition, this study also revealed that IRF-1 modulate Th1 differentiation through establishing IL-12 responsiveness by acting on IL-12 receptor beta1.
  
  
  CONCLUSIONS
  The present data demonstrate that inhibition of IRF-1 obviously decrease the function of Th1 cells and may be a novel participator in the progress of ACS.
authors.affiliation: Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
authors.forename: Min
authors.initials: M
authors.lastname: Guo
authors.forename: Xiaobo
authors.initials: X
authors.lastname: Mao
authors.forename: Qingwei
authors.initials: Q
authors.lastname: Ji
authors.forename: Mingjian
authors.initials: M
authors.lastname: Lang
authors.forename: Songnan
authors.initials: S
authors.lastname: Li
authors.forename: Yudong
authors.initials: Y
authors.lastname: Peng
authors.forename: Wei
authors.initials: W
authors.lastname: Zhou
authors.forename: Bo
authors.initials: B
authors.lastname: Xiong
authors.forename: Qiutang
authors.initials: Q
authors.lastname: Zeng
mesh_terms: D054058:Acute Coronary Syndrome / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D000368:Aged; D015704:CD4 Antigens / Q000096:biosynthesis; D002454:Cell Differentiation / Q000235:genetics; D002478:Cells, Cultured; D002637:Chest Pain; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D004562:Electrocardiography; D005260:Female; D005786:Gene Expression Regulation / Q000276:immunology; D006801:Humans; D050856:Interferon Regulatory Factor-1 / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D018664:Interleukin-12 / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D034741:RNA, Small Interfering / Q000235:genetics; D053707:Receptors, Interleukin-12 / Q000235:genetics / Q000378:metabolism*; D018417:Th1 Cells / Q000276:immunology / Q000378:metabolism* / Q000473:pathology
chemical_list: D015704:CD4 Antigens; D016207:Cytokines; D050856:Interferon Regulatory Factor-1; D034741:RNA, Small Interfering; D053707:Receptors, Interleukin-12; D018664:Interleukin-12