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Immunity
Article
License: Elsevier Non-Commercial
Data sources: UnpayWall
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Immunity
Article . 2007
License: Elsevier Non-Commercial
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Immunity
Article . 2007 . Peer-reviewed
License: Elsevier Non-Commercial
Data sources: Crossref
Immunity
Article . 2008
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Human Leukocyte Antigen-B-Associated Transcript 3 Is Released from Tumor Cells and Engages the NKp30 Receptor on Natural Killer Cells

Authors: Pogge von Strandmann, Elke; Simhadri, Venkateswara Rao; von Tresckow, Bastian; Sasse, Stephanie; Reiners, Katrin S.; Hansen, Hinrich P.; Rothe, Achim; +6 Authors

Human Leukocyte Antigen-B-Associated Transcript 3 Is Released from Tumor Cells and Engages the NKp30 Receptor on Natural Killer Cells

Abstract

The activity of natural killer (NK) cells is regulated by surface receptors, which direct target cell recognition. NKp30 (Natural Cytotoxicity Receptor 3) induces target cell lysis and is also crucial for the interaction with dendritic cells. So far, the cellular ligands for NKp30 have remained elusive. Here we show that the nuclear factor HLA-B-associated transcript 3 (BAT3) was released from tumor cells, bound directly to NKp30, and engaged NKp30 on NK cells. BAT3 triggered NKp30-mediated cytotoxicity and was necessary for tumor rejection in a multiple myeloma model. These data identify BAT3 as a cellular ligand for NKp30. We propose a concept for target cell recognition by NK cells beyond "missing self" and "induced self," mediated through a tumor cell-derived extracellular factor.

Keywords

Cytotoxicity, Immunologic, Natural Cytotoxicity Triggering Receptor 3, Tumor Necrosis Factor-alpha, Immunology, Proteins, Cell Line, Killer Cells, Natural, Interferon-gamma, Infectious Diseases, CELLIMMUNO, Neoplasms, Immunology and Allergy, Humans, Receptors, Immunologic, MOLIMMUNO, Multiple Myeloma, Molecular Chaperones

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    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    298
    popularity
    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
    Top 1%
    influence
    This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    Top 1%
    impulse
    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Top 1%
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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
298
Top 1%
Top 1%
Top 1%
hybrid
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