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. CONCLUSION: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.

journal_name

J Clin Immunol

authors

Guo M,Mao X,Ji Q,Lang M,Li S,Peng Y,Zhou W,Xiong B,Zeng Q

doi

10.1007/s10875-010-9367-8

subject

Has Abstract

pub_date

2010-03-01 00:00:00

pages

241-52

issue

2

eissn

0271-9142

issn

1573-2592

journal_volume

30

pub_type

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