Document Detail


The Th17/Treg imbalance in patients with acute coronary syndrome.
MedLine Citation:
PMID:  18294918     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
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:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-02-21
Journal Detail:
Title:  Clinical immunology (Orlando, Fla.)     Volume:  127     ISSN:  1521-6616     ISO Abbreviation:  Clin. Immunol.     Publication Date:  2008 Apr 
Date Detail:
Created Date:  2008-03-18     Completed Date:  2008-05-20     Revised Date:  2009-12-22    
Medline Journal Info:
Nlm Unique ID:  100883537     Medline TA:  Clin Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  89-97     Citation Subset:  IM    
Affiliation:
Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
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MeSH Terms
Descriptor/Qualifier:
Acute Coronary Syndrome / 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:
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:
Clin Immunol. 2009 Dec;133(3):447

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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