NDLI: Inhibition of IFN Regulatory Factor-1 Down-Regulate Th1 Cell Function in Patients with Acute Coronary Syndrome

Content Provider	Springer Nature Link
Author	Guo, Min Mao, Xiaobo Ji, Qingwei Lang, Mingjian Li, Songnan Peng, Yudong Zhou, Wei Xiong, Bo Zeng, Qiutang
Copyright Year	2010
Abstract	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.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.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 β1.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.
Starting Page	241
Ending Page	252
Page Count	12
File Format	PDF
ISSN	02719142
Journal	Journal of Clinical Immunology
Volume Number	30
Issue Number	2
e-ISSN	15732592
Language	English
Publisher	Springer US
Publisher Date	2010-02-23
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Acute coronary syndrome atherosclerosis IRF-1 Th1 inflammation Medical Microbiology Internal Medicine Infectious Diseases Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Erratum to: TH1/TH2 Functional Imbalance After Acute Myocardial Infarction: Coronary Arterial Inflammation or Myocardial Inflammation

Th1/Th2 Functional Imbalance After Acute Myocardial Infarction: Coronary Arterial Inflammation or Myocardial Inflammation

Coronary Artery Abnormalities in Hyper-IgE Syndrome

Impaired Peripheral Th1 CD4+ T Cell Response to Escherichia coli Proteins in Patients with Crohn’s Disease and Ankylosing Spondylitis

Th2 Responses in OVA-Sensitized BALB/c Mice Are Down-Modulated By Mycobacterium bovis BCG Treatment

Interferon Regulatory Factor (Irf)-1 and Irf-2 Regulate Interferon γ–Dependent Cyclooxygenase 2 Expression

IL-27 is Elevated in Acute Lung Injury and Mediates Inflammation

Downregulation of T helper cell type 3 in patients with acute coronary syndrome.

Trichostatin Differentially Regulates Th1 and Th2 Responses and Alleviates Rheumatoid Arthritis in Mice

Inhibition of IFN Regulatory Factor-1 Down-Regulate Th1 Cell Function in Patients with Acute Coronary Syndrome

Similar Documents

Erratum to: TH1/TH2 Functional Imbalance After Acute Myocardial Infarction: Coronary Arterial Inflammation or Myocardial Inflammation

Th1/Th2 Functional Imbalance After Acute Myocardial Infarction: Coronary Arterial Inflammation or Myocardial Inflammation

Coronary Artery Abnormalities in Hyper-IgE Syndrome

Impaired Peripheral Th1 CD4+ T Cell Response to Escherichia coli Proteins in Patients with Crohn’s Disease and Ankylosing Spondylitis

Th2 Responses in OVA-Sensitized BALB/c Mice Are Down-Modulated By Mycobacterium bovis BCG Treatment

Interferon Regulatory Factor (Irf)-1 and Irf-2 Regulate Interferon γ–Dependent Cyclooxygenase 2 Expression

IL-27 is Elevated in Acute Lung Injury and Mediates Inflammation

Downregulation of T helper cell type 3 in patients with acute coronary syndrome.

Trichostatin Differentially Regulates Th1 and Th2 Responses and Alleviates Rheumatoid Arthritis in Mice

Inhibition of IFN Regulatory Factor-1 Down-Regulate Th1 Cell Function in Patients with Acute Coronary Syndrome