Linked Life Data

11861426

Source:http://linkedlifedata.com/resource/pubmed/id/11861426

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2002-2-25
pubmed:abstractText
Peroxisome proliferator-activated receptors (PPARs) are essential in glucose and lipid metabolism and are implicated in metabolic disorders predisposing to atherosclerosis, such as diabetes and dyslipidemia. Conversely, antidiabetic glitazones and hypolipidemic fibrate drugs, known as PPARgamma and PPARalpha ligands, respectively, reduce the process of atherosclerotic lesion formation, which involves chronic immunoinflammatory processes. Major histocompatibility complex class II (MHC-II) molecules, expressed on the surface of specialized cells, are directly involved in the activation of T lymphocytes and in the control of the immune response. Interestingly, expression of MHC-II has recently been observed in atherosclerotic plaques, and it can be induced by the proinflammatory cytokine interferon-gamma (IFN-gamma) in vascular cells. To explore a possible role for PPAR ligands in the regulation of the immune response, we investigated whether PPAR activation affects MHC-II expression in atheroma-associated cells. In the present study, we demonstrate that PPARgamma but not PPARalpha ligands act as inhibitors of IFN-gamma-induced MHC-II expression and thus as repressors of MHC-II-mediated T-cell activation. All different types of PPARgamma ligands tested inhibit MHC-II. This effect of PPARgamma ligands is due to a specific inhibition of promoter IV of CIITA and does not concern constitutive expression of MHC-II. Thus, the beneficial effects of antidiabetic PPARgamma activators on atherosclerotic plaque development may be partly explained by their repression of MHC-II expression and subsequent inhibition of T-lymphocyte activation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1524-4571
pubmed:author
pubmed:issnType
Electronic
pubmed:day
22
pubmed:volume
90
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
356-62
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:11861426-Arteriosclerosis, pubmed-meshheading:11861426-Cells, Cultured, pubmed-meshheading:11861426-Dose-Response Relationship, Drug, pubmed-meshheading:11861426-Endothelium, Vascular, pubmed-meshheading:11861426-Flow Cytometry, pubmed-meshheading:11861426-Gene Expression Regulation, pubmed-meshheading:11861426-Genes, Reporter, pubmed-meshheading:11861426-Histocompatibility Antigens Class II, pubmed-meshheading:11861426-Humans, pubmed-meshheading:11861426-Hypoglycemic Agents, pubmed-meshheading:11861426-Interferon-gamma, pubmed-meshheading:11861426-Ligands, pubmed-meshheading:11861426-Lymphocyte Activation, pubmed-meshheading:11861426-Lymphocyte Culture Test, Mixed, pubmed-meshheading:11861426-Monocytes, pubmed-meshheading:11861426-Prostaglandin D2, pubmed-meshheading:11861426-RNA, Messenger, pubmed-meshheading:11861426-Receptors, Cytoplasmic and Nuclear, pubmed-meshheading:11861426-T-Lymphocytes, pubmed-meshheading:11861426-Transcription Factors
pubmed:year
2002
pubmed:articleTitle
PPARgamma but not PPARalpha ligands are potent repressors of major histocompatibility complex class II induction in atheroma-associated cells.
pubmed:affiliation
Division of Cardiology, Department of Medicine, University Hospital, Geneva Medical School, Foundation for Medical Research, Geneva, Switzerland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't