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. 2022 Oct 13;13:938306. doi: 10.3389/fimmu.2022.938306

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Copyright © 2022 Haeger, Kridin, Pieper, Griewahn, Nimmerjahn, Zillikens, König, Ludwig and Hundt

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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Proposed model of the contribution of FcγRIV to skin inflammation and blistering in experimental EBA. Treating mice with anti-FcγRIV Ab does not inhibit neutrophil extravasation in antibody transfer-induced EBA mouse model. Although present in the skin, neutrophils are not activated when FcγRIV is blocked, since ROS release is inhibited in vitro and blister formation is inhibited in vivo. Enhanced numbers of neutrophils infiltrating the dermis of anti-FcγRIV Ab-treated mice in the EBA mouse model can be explained by ineffective neutrophil clearance, since missing activation of FcγRIV-blocked neutrophils leads to decreased presentation of “eat-me” signals on the neutrophil surface.