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  • Cutting Edge: Lectin-Like Transcript-1 Is a Ligand for the Inhibitory Human NKR-P1A Receptor

    Author(s)
    B. Rosen, David
    Bettadapura, Jayaram
    Alsharifi, Mohammed
    A. Mathew, Porunelloor
    S. Warren, Hilary
    L. Lanier, Lewis
    Griffith University Author(s)
    Bettadapura, Jayaram
    Year published
    2005
    Metadata
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    Abstract
    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 CD3?-NKR-P1A chimeric receptor; reciprocally, reporter cells with a CD3?-LLT1 chimeric receptor are stimulated by NKR-P1A. Moreover, LLT1 on target ...
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    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 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.
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    Journal Title
    Journal of Immunology
    Volume
    175
    Publisher URI
    http://www.ncbi.nlm.nih.gov/pubmed/16339513
    Subject
    Innate Immunity
    Immunology
    Publication URI
    http://hdl.handle.net/10072/39290
    Collection
    • Journal articles

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