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dc.contributor.authorB. Rosen, David
dc.contributor.authorBettadapura, Jayaram
dc.contributor.authorAlsharifi, Mohammed
dc.contributor.authorA. Mathew, Porunelloor
dc.contributor.authorS. Warren, Hilary
dc.contributor.authorL. Lanier, Lewis
dc.date.accessioned2017-05-03T16:00:59Z
dc.date.available2017-05-03T16:00:59Z
dc.date.issued2005
dc.date.modified2011-06-29T08:09:26Z
dc.identifier.issn00221767
dc.identifier.urihttp://hdl.handle.net/10072/39290
dc.description.abstractIncreasingly, 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 CD3?-NKR-P1A chimeric receptor; reciprocally, reporter cells with a CD3?-LLT1 chimeric receptor are stimulated by NKR-P1A. Moreover, LLT1 on target cells can inhibit NK cytotoxicity via interactions with NKR-P1A.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.languageEnglish
dc.language.isoeng
dc.publisherThe American Association of Immunologists
dc.publisher.placeUSA
dc.publisher.urihttp://www.ncbi.nlm.nih.gov/pubmed/16339513
dc.relation.ispartofstudentpublicationN
dc.relation.ispartofpagefrom7796
dc.relation.ispartofpageto7799
dc.relation.ispartofjournalJournal of Immunology
dc.relation.ispartofvolume175
dc.rights.retentionY
dc.subject.fieldofresearchInnate Immunity
dc.subject.fieldofresearchImmunology
dc.subject.fieldofresearchcode110707
dc.subject.fieldofresearchcode1107
dc.titleCutting Edge: Lectin-Like Transcript-1 Is a Ligand for the Inhibitory Human NKR-P1A Receptor
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.date.issued2005
gro.hasfulltextNo Full Text
gro.griffith.authorBettadapura, Jayaram


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