| Autor: |
Domaica CI; Institute of Biology and Experimental Medicine (IBYME), National Research Council (CONICET), Ciudad de Buenos Aires, Argentina., Fuertes MB, Rossi LE, Girart MV, Avila DE, Rabinovich GA, Zwirner NW |
| Jazyk: |
angličtina |
| Zdroj: |
EMBO reports [EMBO Rep] 2009 Aug; Vol. 10 (8), pp. 908-15. Date of Electronic Publication: 2009 Jun 05. |
| DOI: |
10.1038/embor.2009.92 |
| Abstrakt: |
Natural killer (NK) cells trigger cytotoxicity and interferon (IFN)-gamma 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-gamma 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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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