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. 2019 Jul 4;10:1453. doi: 10.3389/fimmu.2019.01453

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Copyright © 2019 Liu, Gorzelanny and Schneider.

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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Platelets involvement in the pathogenesis of AAVs. Neutrophils play a crucial role in the development of AAVs. Platelet receptors CD40L and P-selectin enable the interaction with neutrophils promoting ROS generation and NET formation. ROS and NETs are toxic to the endothelium and can lead to VWF release and vascular injury. VWF is well-known to mediate platelets adhesion and aggregation. Similar to neutrophils, sCD40L-CD40 can also mediate platelet -endothelial cell interaction, which can enhance the expression of endothelial cell adhesion proteins (e.g., E-selectin, VCAM-1, and ICAM-1). C5a, a chemoattractant anaphylatoxin, can directly attract and activate neutrophils promoting the exposure of tissue factor. Tissue factor initiates the plasmatic coagulation which culminates in the generation of thrombin. Thrombin is able to further activate platelets and endothelial cells through PAR signaling pathway, followed by platelet degranulation and VWF release. In addition, C5a can also directly active endothelial cells accelerating vascular injury.