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. 2019 Jun 3;10:2402. doi: 10.1038/s41467-019-10360-4

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — EVs play critical roles in the pathogenesis of viral infectons. DV activates macrophages and neutrophils via CLEC5A. DV also stimulate CLEC2 on platelets to promote release of EVs (DV-EXOs and DV-MVs), which further enhance the secretion of proinflammatory cytokines and NET formation in neutrophils via CLEC5A and TLR2