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. 2016 Sep 21;7:373. doi: 10.3389/fimmu.2016.00373

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Copyright © 2016 Olsson and Cedervall.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Platelet–neutrophil crosstalk in tumor-induced NETosis. Tumor cells can directly induce NETosis in an individual with cancer by secretion of factors such as G-CSF and IL-8. Tumors furthermore promote platelet activation, for example, by production of tissue factor (TF). Activated platelets function as inducers of NETosis. This effect is mediated via direct binding of P-selectin on activated platelets and PSGL-1 on neutrophils. Stimulation of platelets via toll-like receptor 4 (TLR4), by LPS during infectious disease or tumor-derived factors, possibly fibronectin ED-A, may further contribute to platelet-induced NETosis. NETs further stimulate platelet activation and thrombosis due to externalized chromatin and localization of TF and factor XII.