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. 2022 Aug 1;13:953129. doi: 10.3389/fimmu.2022.953129

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Copyright © 2022 Wienkamp, Erpenbeck and Rossaint

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) and the copyright owner(s) 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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Pathogen-induced platelet-mediated NET formation. Staphylococcus aureus α-toxin induces pore formation in platelets, which then release hBD-1. Gramnegative bacteria and LPS activate platelets in a TLR4-dependent manner, and blocking of LFA-1 in this background abrogated NETosis in neutrophils. Dengue viruses can be sensed by platelets via CLEC2, which leads to shedding of extracellular vesicles promoting NETosis in a TLR2- and CLEC5A-dependent manner. Inlfuenza A virus are recognized via TLR7, and granular C3 then induces NETosis in neutrophils. C3, complement C3; CLEC2, C-type lectin-like receptor 2; CLEC5A, C-type lectin domain containing 5A; hBD-1, human β-defensin 1; ICAM, intercellular adhesion molecule; LFA-1, leukocyte function-associated antigen 1; LPS, lipopolysaccharide; TLR, toll-like receptor.