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Tumour‐experienced T cells promote NK cell activity through trogocytosis of NKG2D and NKp46 ligands
Author(s) -
Domaica Carolina I,
Fuertes Mercedes B,
Rossi Lucas E,
Girart María V,
Ávila Damián E,
Rabinovich Gabriel A,
Zwirner Norberto W
Publication year - 2009
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1038/embor.2009.92
Subject(s) - nkg2d , degranulation , biology , microbiology and biotechnology , interleukin 21 , natural killer cell , cytotoxicity , lymphokine activated killer cell , cytotoxic t cell , natural killer t cell , interleukin 12 , secretion , cd8 , cell , effector , immunology , receptor , immune system , in vitro , biochemistry
Natural killer (NK) cells trigger cytotoxicity and interferon (IFN)‐γ secretion on engagement of the natural‐killer group (NKG)2D receptor or members of the natural cytotoxicity receptor (NCR) family, such as NKp46, by ligands expressed on tumour cells. However, it remains unknown whether T cells can regulate NK cell‐mediated anti‐tumour responses. Here, we investigated the early events occurring during T cell–tumour cell interactions, and their impact on NK cell functions. We observed that on co‐culture with some melanomas, activated CD4 + T cells promoted degranulation, and NKG2D‐ and NKp46‐dependent IFN‐γ secretion by NK cells, probably owing to the capture of NKG2D and NKp46 ligands from the tumour‐cell surface (trogocytosis). This effect was observed in CD4 + , CD8 + and resting T cells, which showed substantial amounts of cell surface major histocompatibility complex class I chain‐related protein A on co‐culture with tumour cells. Our findings identify a new, so far, unrecognized mechanism by which effector T cells support NK cell function through the capture of specific tumour ligands with profound implications at the crossroad of innate and adaptive immunity.

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