rdf:type |
|
lifeskim:mentions |
umls-concept:C0011306,
umls-concept:C0017262,
umls-concept:C0032854,
umls-concept:C0035647,
umls-concept:C0185117,
umls-concept:C0205252,
umls-concept:C0591833,
umls-concept:C1561558,
umls-concept:C1621296,
umls-concept:C1880177,
umls-concept:C2911684
|
pubmed:issue |
3
|
pubmed:dateCreated |
2007-4-6
|
pubmed:abstractText |
Recent data have revealed that Ag presentation by immature dendritic cells (imDCs) plays a role in establishing and maintaining T-cell tolerance, but the mechanism remains unclear. PD-L1 and PD-L2, ligands for programmed-death receptor 1 (PD-1), members of the expanding B7 family, were highlighted for their inhibitory role in T-cell responses. Here, we show that blockade of PD-1 ligands on imDCs resulted in enhanced T-cell proliferation, which is perhaps due to the enhancement of IL-2 production from DC-stimulated T cells. PD-1 ligands blockade on mDCs did not show a significant stimulatory effect as markedly as imDCs. The inhibitory effects of PD-1 ligands would be dependent on maturation status of DCs, where attenuated positive costimulatory molecules provided the opportunity for PD-1 ligands to exert their strong capacity. Our data are consistent with the hypothesis that imDCs have an inhibitory bias, and indicate that PD-L1 and PD-L2 contribute to the poor stimulatory capacity of imDCs.
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD274,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD80,
http://linkedlifedata.com/resource/pubmed/chemical/Cd274 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Ligands,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Pdcd1lg2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/Programmed Cell Death 1 Ligand 2...
|
pubmed:status |
MEDLINE
|
pubmed:issn |
0171-2985
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
212
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
159-65
|
pubmed:dateRevised |
2011-11-17
|
pubmed:meshHeading |
pubmed-meshheading:17412283-Animals,
pubmed-meshheading:17412283-Antigens, CD274,
pubmed-meshheading:17412283-Antigens, CD80,
pubmed-meshheading:17412283-Cell Differentiation,
pubmed-meshheading:17412283-Cells, Cultured,
pubmed-meshheading:17412283-Dendritic Cells,
pubmed-meshheading:17412283-Female,
pubmed-meshheading:17412283-Immune Tolerance,
pubmed-meshheading:17412283-Ligands,
pubmed-meshheading:17412283-Lymphocyte Activation,
pubmed-meshheading:17412283-Membrane Glycoproteins,
pubmed-meshheading:17412283-Mice,
pubmed-meshheading:17412283-Mice, Inbred C57BL,
pubmed-meshheading:17412283-Peptides,
pubmed-meshheading:17412283-Programmed Cell Death 1 Ligand 2 Protein,
pubmed-meshheading:17412283-T-Lymphocytes
|
pubmed:year |
2007
|
pubmed:articleTitle |
Expression of programmed-death receptor ligands 1 and 2 may contribute to the poor stimulatory potential of murine immature dendritic cells.
|
pubmed:affiliation |
Clinical Immunology Laboratory of Jiangsu Province, Suzhou University No. 1 Affiliated Hospital, 96 Shizi Street, Suzhou 215006, China.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|