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http://purl.uniprot.org/citations/20177960http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20177960http://www.w3.org/2000/01/rdf-schema#comment"

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."xsd:string
http://purl.uniprot.org/citations/20177960http://purl.org/dc/terms/identifier"doi:10.1007/s10875-010-9367-8"xsd:string
http://purl.uniprot.org/citations/20177960http://purl.uniprot.org/core/author"Guo M."xsd:string
http://purl.uniprot.org/citations/20177960http://purl.uniprot.org/core/author"Li S."xsd:string
http://purl.uniprot.org/citations/20177960http://purl.uniprot.org/core/author"Mao X."xsd:string
http://purl.uniprot.org/citations/20177960http://purl.uniprot.org/core/author"Zeng Q."xsd:string
http://purl.uniprot.org/citations/20177960http://purl.uniprot.org/core/author"Zhou W."xsd:string
http://purl.uniprot.org/citations/20177960http://purl.uniprot.org/core/author"Xiong B."xsd:string
http://purl.uniprot.org/citations/20177960http://purl.uniprot.org/core/author"Lang M."xsd:string
http://purl.uniprot.org/citations/20177960http://purl.uniprot.org/core/author"Peng Y."xsd:string
http://purl.uniprot.org/citations/20177960http://purl.uniprot.org/core/author"Ji Q."xsd:string
http://purl.uniprot.org/citations/20177960http://purl.uniprot.org/core/date"2010"xsd:gYear
http://purl.uniprot.org/citations/20177960http://purl.uniprot.org/core/name"J Clin Immunol"xsd:string
http://purl.uniprot.org/citations/20177960http://purl.uniprot.org/core/pages"241-252"xsd:string
http://purl.uniprot.org/citations/20177960http://purl.uniprot.org/core/title"Inhibition of IFN regulatory factor-1 down-regulate Th1 cell function in patients with acute coronary syndrome."xsd:string
http://purl.uniprot.org/citations/20177960http://purl.uniprot.org/core/volume"30"xsd:string
http://purl.uniprot.org/citations/20177960http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/20177960
http://purl.uniprot.org/citations/20177960http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/20177960
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