Linked Life Data

15226269

Source:http://linkedlifedata.com/resource/pubmed/id/15226269

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2004-7-19
pubmed:abstractText
Endothelial cells have been shown to activate T cell responses to alloantigens, triggering transplant rejection. However, they may also play a role in tolerance induction. Using RT-PCR we show here that alloantigen specific CD8(+)CD28(-) T suppressor cells generated in vitro are FOXP3 positive and interact with human endothelial cells. This interaction results in the induction of inhibitory receptors and down-regulation of costimulatory and adhesion molecules, thus rendering endothelial cells tolerogenic. In turn, tolerized endothelial cells elicit the differentiation of CD8(+)CD28(-) FOXP3(+) T suppressor cells. Taken together our data demonstrate a functional and phenotypic overlap between tolerogenic dendritic cells and endothelial cells. Furthermore, alloantigen specific CD8(+)CD28(-) FOXP3(+) T cells, which trigger the upregulation of inhibitory receptors in endothelial cells, are present in the circulation of heart allograft recipients in quiescence as demonstrated by flow cytometry, RT-PCR and luciferase transcription assays. Their detection facilitates the identification of patients who may benefit from partial or complete cessation of immunosuppressive therapy, a goal of obvious importance given the morbidity and mortality associated with chronic immunosuppression. Modulation of endothelial cells in favor of promoting tolerance may be important for long-term survival of organ allografts.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0953-8178
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1055-68
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:15226269-Adult, pubmed-meshheading:15226269-Antigens, CD28, pubmed-meshheading:15226269-Base Sequence, pubmed-meshheading:15226269-Cell Communication, pubmed-meshheading:15226269-Cell Differentiation, pubmed-meshheading:15226269-Cells, Cultured, pubmed-meshheading:15226269-Endothelial Cells, pubmed-meshheading:15226269-Female, pubmed-meshheading:15226269-Heart Transplantation, pubmed-meshheading:15226269-Humans, pubmed-meshheading:15226269-Immune Tolerance, pubmed-meshheading:15226269-Immunosuppression, pubmed-meshheading:15226269-Isoantigens, pubmed-meshheading:15226269-Male, pubmed-meshheading:15226269-Membrane Glycoproteins, pubmed-meshheading:15226269-Middle Aged, pubmed-meshheading:15226269-Molecular Sequence Data, pubmed-meshheading:15226269-Receptors, Cell Surface, pubmed-meshheading:15226269-Receptors, Immunologic, pubmed-meshheading:15226269-T-Lymphocytes, Regulatory, pubmed-meshheading:15226269-Transplantation, Homologous
pubmed:year
2004
pubmed:articleTitle
Alloantigen specific CD8+CD28- FOXP3+ T suppressor cells induce ILT3+ ILT4+ tolerogenic endothelial cells, inhibiting alloreactivity.
pubmed:affiliation
Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't