干扰素调节因子-1对急性冠脉综合征患者Th分化影响及其机制研究-内科学(心血管专业)专业论文.docx

华中科技大学博士学位论文 华 中 科 技 大 学 博 士 学 位 论 文 PAGE 4 PAGE 4 The Effect and mechanism of IFN Regulatory Factor-1 on T helper lymphocyte differentiation in patients with acute coronary syndrome Department of Cardiology, the Union Hospital, Tongji Medical College，Huazhong University of Science and Technology; Wuhan, China Ph. D Candidate: Guo Min Supervisor: Zeng Qiutang Abstracts Part Ⅰ The expression of IFN Regulatory Factor-1 and cytokines related to CD4+ T cells in patients with acute coronary syndrome Aim: IFN regulatory factor (IRF)-1 is a pleiotropic transcription factor involved in autoimmune disease. The aim of the study was to investigate the expression of IRF-1 in CD4+ T cells and explore the possible role of IRF-1 in AS and ACS. Methods: Patients with clinical presentation of chest pain (CPS), stable angina (SA), unstable angina (UA) and acute myocardial infarction (AMI) were enrolled in this study. CD4+ T cells were enriched and analyzed for the expression of IRF-1. The concentrations of plasma Th1 cytokines IFN-γ、TNF-α、IL-12 and Treg related cytokines TGF-β1 and IL-10 were detected by ELISA. The correlation between IRF-1 and cytokines were analyzed by Pearson correlation analysis. Results: The results demonstrated that the expression of IRF-1 in CD4+ T cells was significantly increased in patients with ACS. The expression of IRF-1 were positively correlated with plasma Th1 cytokines and negatively correlated with plasma Treg related cytokines. Conclusion: The present data demonstrate that the up-regulation of IRF-1 may be one of the mechanisms in the onset of ACS. It may play a potential role in the differentiation of Th cells in ACS and may be a novel therapeutic target for ACS. Keywords: atherosclerosis; acute coronary syndrome; IRF-1; cytokine Part Ⅱ The Effect of IRF-1 siRNA on the differentiation of Th cells in patients with acute coronary syndrome Aim: The crucial role of Th cells in atherosclerosis in no longer controversial. The aim of the study was to i