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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
12
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pubmed:dateCreated |
2005-12-12
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pubmed:abstractText |
Increasingly, roles are emerging for C-type lectin receptors in immune regulation. One receptor whose function has remained largely enigmatic is human NKR-P1A (CD161), present on NK cells and subsets of T cells. In this study, we demonstrate that the lectin-like transcript-1 (LLT1) is a physiologic ligand for NKR-P1A. LLT1-containing liposomes bind to NKR-P1A+ cells, and binding is inhibited by anti-NKR-P1A mAb. Additionally, LLT1 activates NFAT-GFP reporter cells expressing a CD3zeta-NKR-P1A chimeric receptor; reciprocally, reporter cells with a CD3zeta-LLT1 chimeric receptor are stimulated by NKR-P1A. Moreover, LLT1 on target cells can inhibit NK cytotoxicity via interactions with NKR-P1A.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD3,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Surface,
http://linkedlifedata.com/resource/pubmed/chemical/CD3 antigen, zeta chain,
http://linkedlifedata.com/resource/pubmed/chemical/CLEC2D protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Green Fluorescent Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/KLRB1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Lectins, C-Type,
http://linkedlifedata.com/resource/pubmed/chemical/Ligands,
http://linkedlifedata.com/resource/pubmed/chemical/Liposomes,
http://linkedlifedata.com/resource/pubmed/chemical/NFATC Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/NK Cell Lectin-Like Receptor...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Fusion Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0022-1767
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
175
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
7796-9
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:16339513-Animals,
pubmed-meshheading:16339513-Antigens, CD3,
pubmed-meshheading:16339513-Antigens, Surface,
pubmed-meshheading:16339513-Cells, Cultured,
pubmed-meshheading:16339513-Cytotoxicity, Immunologic,
pubmed-meshheading:16339513-Green Fluorescent Proteins,
pubmed-meshheading:16339513-Humans,
pubmed-meshheading:16339513-Killer Cells, Natural,
pubmed-meshheading:16339513-Lectins, C-Type,
pubmed-meshheading:16339513-Ligands,
pubmed-meshheading:16339513-Liposomes,
pubmed-meshheading:16339513-Lymphocyte Activation,
pubmed-meshheading:16339513-Mice,
pubmed-meshheading:16339513-NFATC Transcription Factors,
pubmed-meshheading:16339513-NK Cell Lectin-Like Receptor Subfamily B,
pubmed-meshheading:16339513-Protein Binding,
pubmed-meshheading:16339513-Receptors, Cell Surface,
pubmed-meshheading:16339513-Recombinant Fusion Proteins,
pubmed-meshheading:16339513-T-Lymphocyte Subsets,
pubmed-meshheading:16339513-Transfection
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pubmed:year |
2005
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pubmed:articleTitle |
Cutting edge: lectin-like transcript-1 is a ligand for the inhibitory human NKR-P1A receptor.
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pubmed:affiliation |
Department of Microbiology and Immunology, The Cancer Research Institute, and Biomedical Sciences Graduate Program, University of California, San Francisco, CA 94143, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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