Linked Life Data

20511710

Source:http://linkedlifedata.com/resource/pubmed/id/20511710

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2010-5-31
pubmed:abstractText
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-kappaB 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-kappaB signaling pathway.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1421-9778
pubmed:author
pubmed:copyrightInfo
Copyright 2010 S. Karger AG, Basel.
pubmed:issnType
Electronic
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
649-56
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Oxidized low-density lipoprotein-induced proinflammatory cytokine response in macrophages are suppressed by CD4CD25(+)Foxp3(+) regulatory T cells through downregulating toll like receptor 2-mediated activation of NF-kappaB.
pubmed:affiliation
Department of Cardiology, Institute of Cardiovascular Diseases, Union Hospital, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't