• Corpus ID: 14537110

Lysis of tumor cells by natural killer cells in mice is impeded by platelets.

@article{Nieswandt1999LysisOT,
  title={Lysis of tumor cells by natural killer cells in mice is impeded by platelets.},
  author={Bernhard Nieswandt and Michael Hafner and Bernd Echtenacher and Daniela N M{\"a}nnel},
  journal={Cancer research},
  year={1999},
  volume={59 6},
  pages={
          1295-300
        }
}
Natural killer (NK) cells provide effective antitumoral activity in the blood stream of mice, leading to reduced metastasis. There are, however, tumor cells that metastasize despite the presence of an intact NK system. The capability of tumor cells to induce platelet aggregation, on the other hand, correlates with their enhanced metastatic potential. A counteractive role of platelets for the NK function in metastasis has never been conceived. Here we demonstrate for the first time that… 
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The available data regarding tumor-platelet-NK cell interaction focusing on metastatic tumor spread is reviewed and the molecular mechanisms underlying this trilateral crosstalk are discussed.
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The known interactions between platelets and NK cells in the solid tumor setting are reviewed and discussed and how these could also apply to hematological cancers.
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The underlying mechanisms of NK cell control by platelets and myeloid cells with focus on NKG2D and its ligands are discussed, and a timely perspective on how to harness these pathways with novel immunotherapeutic approaches is provided.
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It is shown that platelet-derived soluble factors, secreted on coating of tumor cells or after stimulation with classic platelet agonists, impair NK cell antitumor reactivity resulting in diminished granule mobilization, cytotoxicity, and IFN-gamma production, and therapeutic intervention in tumor cell-platelet interaction and the resulting TGF-beta release by platelets may serve to enhance antitumors immunity.
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It is concluded that Cil-L reduced metastasis by restricting the aggregability of mouse platelets, which probably prevents the interaction between circulating 4T1 tumor cells and Platelets, making the Cil -L a useful tool for the inhibition of breast cancer metastasis in mice.
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