Platelets and fibrin(ogen) increase metastatic potential by impeding natural killer cell–mediated elimination of tumor cells
作者： Joseph S. Palumbo , Kathryn E. Talmage , Jessica V. Massari , Christine M. La Jeunesse , Matthew J. Flick
DOI: 10.1182/BLOOD-2004-06-2272
关键词: Fibrin 、 Fibrinogen 、 Innate immune system 、 Circulating tumor cell 、 Natural killer cell 、 Platelet 、 Platelet activation 、 Biology 、 Lymphokine-activated killer cell 、 Immunology
摘要: To test the hypothesis that platelet activation contributes to tumor dissemination, we studied metastasis in mice lacking Galphaq, a G protein critical for activation. Loss of resulted profound diminution both experimental and spontaneous metastases. Analyses distribution radiolabeled cells demonstrated function, like fibrinogen, significantly improved survival circulating pulmonary vasculature. More detailed studies showed increase metastatic success conferred by either platelets or fibrinogen was linked natural killer cell function. Specifically, pronounced reduction observed fibrinogen- Galphaq-deficient relative control animals eliminated immunologic genetic depletion cells. These establish an important link between hemostatic factors innate immunity indicate one mechanism which platelet-fibrin(ogen) axis potential is impeding elimination
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