| The Th17/Treg imbalance in patients with acute coronary syndrome. | |
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MedLine Citation:
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PMID: 18294918 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Atherosclerosis is a chronic inflammatory disease regulated by T lymphocyte subsets. Recently, CD4+CD25+Foxp3+ regulatory T (Treg) cells and Th17 cells have been described as two distinct subsets from Th1 and Th2 cells and have the opposite effects on autoimmunity. Th17/Treg balance controls inflammation and may be important in the pathogenesis of plaque destabilization and the onset of acute coronary syndrome [ACS, including unstable angina (UA) and acute myocardial infarction (AMI)]. To assess whether this balance was broken in patients with coronary heart disease, we detected Th17/Treg functions on different levels including cell frequencies, related cytokine secretion and key transcription factors in patients with AMI, UA, stable angina (SA) and controls. The results demonstrated that patients with ACS revealed significant increase in peripheral Th17 number, Th17 related cytokines (IL-17, IL-6 and IL-23) and transcription factor (RORgammat) levels and obvious decrease in Treg number, Treg related cytokines (IL-10 and TGF-beta1) and transcription factor (Foxp3) levels as compared with patients with SA and controls. Results indicate that Th17/Treg functional imbalance exists in patients with ACS, suggesting a potential role for Th17/Treg imbalance in plaque destabilization and the onset of ACS. |
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Authors:
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Xiang Cheng; Xian Yu; Ying-Jun Ding; Qing-Qing Fu; Jiang-Jiao Xie; Ting-Ting Tang; Rui Yao; Yong Chen; Yu-Hua Liao |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2008-02-21 |
Journal Detail:
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Title: Clinical immunology (Orlando, Fla.) Volume: 127 ISSN: 1521-6616 ISO Abbreviation: Clin. Immunol. Publication Date: 2008 Apr |
Date Detail:
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Created Date: 2008-03-18 Completed Date: 2008-05-20 Revised Date: 2009-12-22 |
Medline Journal Info:
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Nlm Unique ID: 100883537 Medline TA: Clin Immunol Country: United States |
Other Details:
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Languages: eng Pagination: 89-97 Citation Subset: IM |
Affiliation:
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Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acute Coronary Syndrome
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immunology*,
metabolism Enzyme-Linked Immunosorbent Assay Female Flow Cytometry Forkhead Transcription Factors / immunology, metabolism Gene Expression Humans Interleukin-10 / immunology, metabolism Interleukin-17 / immunology, metabolism Interleukin-23 / immunology, metabolism Interleukin-6 / immunology, metabolism Male Middle Aged Nuclear Receptor Subfamily 1, Group F, Member 3 Receptors, Retinoic Acid / immunology, metabolism Receptors, Thyroid Hormone / immunology, metabolism Reverse Transcriptase Polymerase Chain Reaction T-Lymphocyte Subsets / immunology*, metabolism T-Lymphocytes, Helper-Inducer / immunology*, metabolism T-Lymphocytes, Regulatory / immunology*, metabolism Transforming Growth Factor beta1 / immunology, metabolism |
| Chemical | |
Reg. No./Substance:
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0/FOXP3 protein, human; 0/Forkhead Transcription Factors; 0/Interleukin-17; 0/Interleukin-23; 0/Interleukin-6; 0/Nuclear Receptor Subfamily 1, Group F, Member 3; 0/RORC protein, human; 0/Receptors, Retinoic Acid; 0/Receptors, Thyroid Hormone; 0/Transforming Growth Factor beta1; 130068-27-8/Interleukin-10 |
| Comments/Corrections | |
Erratum In:
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Clin Immunol. 2009 Dec;133(3):447 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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