Source:http://linkedlifedata.com/resource/pubmed/id/18929847
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions |
umls-concept:C0014257,
umls-concept:C0017262,
umls-concept:C0167627,
umls-concept:C0185117,
umls-concept:C0220825,
umls-concept:C1332709,
umls-concept:C1366561,
umls-concept:C1413243,
umls-concept:C1515895,
umls-concept:C1539081,
umls-concept:C1704259,
umls-concept:C1704675,
umls-concept:C1705987,
umls-concept:C1998811,
umls-concept:C2911684
|
pubmed:issue |
8
|
pubmed:dateCreated |
2008-10-20
|
pubmed:abstractText |
This study was designed to examine the role of monocyte-derived CD80 in providing costimulation to CD4+ cells, and to determine whether monocyte-derived CD80 expression is regulated by CD86/CD28 and CD40/CD154 pathways during allogeneic immunoresponses. Human endothelial cells (EC) and purified monocytes cocultured with or without CD4+ cells were analyzed by real-time quantitative polymerase chain reaction (RT-PCR) and florescence-activated cell scanning (FACS). Peripheral blood mononuclear cells (PBMC)-EC cocultures with or without costimulation blockade were analyzed by FACS. The effects of CD154 and CD28 blockade to inhibit lymphocyte proliferation were evaluated by mixed lymphocyte-EC reaction (MLER). RT-PCR demonstrated upregulation of CD80 transcripts in EC-stimulated monocytes in the absence of CD4+ cells. However, the surface expression of CD80 was undetectable. The expression of CD80 was restored in the presence of CD4+ cells. Additionally, CD80 blockade partially inhibited CD4+ cell proliferation induced by EC-conditioned monocytes. Monocytes demonstrated upregulation of CD80 on the surface during PBMC-EC interaction. CD86, CD28, and CD154 blockade did not prevent upregulation of monocyte-derived CD80 expression. CD28 and CD154 blockade partially inhibited lymphocyte proliferation of MLER. In summary, EC-stimulated monocytes upregulated CD80 expression at the transcript level but not on their surface in the absence of T cells. The surface expression of monocyte-derived CD80 is upregulated on EC-stimulated monocytes in the presence of T cells. CD154/CD40 and CD28/CD86 blockade cannot prevent monocyte-derived CD80 expression, suggesting that CD80 upregulation is through a CD154- or CD86-independent pathway. Specific therapy to prevent monocyte activation may be required for successful allograft transplantation.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD28,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD40,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD80,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD86,
http://linkedlifedata.com/resource/pubmed/chemical/CD40 Ligand
|
pubmed:status |
MEDLINE
|
pubmed:month |
Oct
|
pubmed:issn |
0041-1345
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
40
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
2729-33
|
pubmed:meshHeading |
pubmed-meshheading:18929847-Antigens, CD,
pubmed-meshheading:18929847-Antigens, CD28,
pubmed-meshheading:18929847-Antigens, CD40,
pubmed-meshheading:18929847-Antigens, CD80,
pubmed-meshheading:18929847-Antigens, CD86,
pubmed-meshheading:18929847-Aorta,
pubmed-meshheading:18929847-CD4-Positive T-Lymphocytes,
pubmed-meshheading:18929847-CD40 Ligand,
pubmed-meshheading:18929847-Endothelium, Vascular,
pubmed-meshheading:18929847-Gene Expression Regulation,
pubmed-meshheading:18929847-Humans,
pubmed-meshheading:18929847-Lymphocyte Activation,
pubmed-meshheading:18929847-Monocytes,
pubmed-meshheading:18929847-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:18929847-Transcription, Genetic,
pubmed-meshheading:18929847-Up-Regulation
|
pubmed:year |
2008
|
pubmed:articleTitle |
Evaluation of CD86/CD28 and CD40/CD154 pathways in regulating monocyte-derived CD80 expression during their interaction with allogeneic endothelium.
|
pubmed:affiliation |
Department of Transplantation, Jinan City Central Hospital, P.R. China.
|
pubmed:publicationType |
Journal Article
|