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Original Paper

Oxidized Low-density Lipoprotein-induced Proinflammatory Cytokine Response in Macrophages are Suppressed by CD4+CD25+Foxp3+ Regulatory T Cells Through Downregulating Toll Like Receptor 2-mediated Activation of NF-κB

Li M.1 · Lin J.1 · Wang Z.1 · He S.1 · Ma X.1 · Li D.1

Author affiliations

Department of Cardiology, Institute of Cardiovascular Diseases, Union Hospital, Tongji Medical College, Huazhong University of Science & Technology, Wuhan,1These authors contributed equally to this work

Corresponding Author

Dazhu Li

Department of Cardiology, Institute of Cardiovascular Diseases

Union Hospital, Tongji Medical College

Huazhong University of Science and Technology, Wuhan (China)

E-Mail lidazhuhp@sohu.com

Related Articles for ""

Cell Physiol Biochem 2010;25:649–656

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Abstract

CD4+CD25+ regulatory T cells (Tregs) exert a suppressive activity on atherosclerosis but the underlying mechanism remains unclear. Here, we investigated whether and how Tregs affect oxLDL-induced proinflammatory response in macrophages. Tregs were isolated by magnetic cell sorting-column and analyzed by flow cytometry. Macrophages were cultured with or without Tregs in the presence of oxLDL for 48 hours to induce proinflammatory response. Our data showed that with oxLDL challenge, the Treg-modulated macrophages have decreased NO production and iNOS expression, decreased HLA-DR and CD86 expression, and down-regulated proinflammatory cytokine/chemokine production. Tregs can inhibit the pro-inflammatory properties of macrophages and steer macrophage differentiation toward an anti-inflammatory cytokine producing phenotype. Mechanistic studies reveal that Treg-mediated suppression of the monocyte response to oxLDL was reflected by a reduction in the up-regulation of NF-ĸB activity accompanied by a decreased expression of TLR2 but not TLR4 at the transcriptional level. These results suggest that CD4+CD25+Foxp3+ regulatory T cells may exert its suppressive functions on pro-inflammatory properties of OxLDL induced-macrophages partly through TLR2-NF-ĸB signaling pathway.

© 2010 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Accepted: April 07, 2010
Published online: May 18, 2010
Issue release date: January 2006

Number of Print Pages: 8
Number of Figures: 0
Number of Tables: 0

ISSN: 1015-8987 (Print)
eISSN: 1421-9778 (Online)

For additional information: https://www.karger.com/CPB


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