SHP-1-mediated inhibitory signals promote responsiveness and anti-tumour functions of natural killer cells

Charlotte Viant, Aurore Fenis, Gaëtan Chicanne, Bernard Payrastre, Sophie Ugolini () and Eric Vivier ()
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Charlotte Viant: Centre d’Immunologie de Marseille-Luminy, Aix-Marseille University UM2, Parc Scientifique et Technologique de Luminy, Case 906
Aurore Fenis: Centre d’Immunologie de Marseille-Luminy, Aix-Marseille University UM2, Parc Scientifique et Technologique de Luminy, Case 906
Gaëtan Chicanne: INSERM, U1048 and Université Toulouse III, Institut de Maladies Métaboliques et Cardiovasculaires, CHU-Rangueil
Bernard Payrastre: INSERM, U1048 and Université Toulouse III, Institut de Maladies Métaboliques et Cardiovasculaires, CHU-Rangueil
Sophie Ugolini: Centre d’Immunologie de Marseille-Luminy, Aix-Marseille University UM2, Parc Scientifique et Technologique de Luminy, Case 906
Eric Vivier: Centre d’Immunologie de Marseille-Luminy, Aix-Marseille University UM2, Parc Scientifique et Technologique de Luminy, Case 906

Nature Communications, 2014, vol. 5, issue 1, 1-11

Abstract: Abstract Natural killer (NK) cells are cytotoxic innate lymphoid cells that are involved in immune defense. NK cell reactivity is controlled in part by MHC class I recognition by inhibitory receptors, but the underlying molecular mechanisms remain undefined. Using a mouse model of conditional deletion in NK cells, we show here that the protein tyrosine phosphatase SHP-1 is essential for the inhibitory function of NK cell MHC class I receptors. In the absence of SHP-1, NK cells are hyporesponsive to tumour cells in vitro and their early Ca2+ signals are compromised. Mice without SHP-1 in NK cells are unable to reject MHC class I-deficient transplants and to control tumours in vivo. Thus, the inhibitory activity of SHP-1 is needed for setting the threshold of NK cell reactivity.

Date: 2014
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DOI: 10.1038/ncomms6108

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