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CORRECTION article

Front. Immunol., 06 October 2022
Sec. Molecular Innate Immunity
This article is part of the Research Topic Neutrophil Death Regulation in Critical Illness View all 11 articles

Corrigendum: PD-L1 maintains neutrophil extracellular traps release by inhibiting neutrophil autophagy in endotoxin-induced lung injury

  • Faculty of Anesthesiology, Changhai Hospital, the Naval Medical University, Shanghai, China

A Corrigendum on
PD-L1 maintains neutrophil extracellular traps release by inhibiting neutrophil autophagy in endotoxin-induced lung injury.

by Zhu C-l, Xie J, Zhao Z-z, Li P, Liu Q, Guo Y, Meng Y, Wan X-j, Bian J-j, Deng X-m and Wang J-f (2022) Front. Immunol. 13:949217. doi: 10.3389/fimmu.2022.949217

In the published article, there was an error in Figure 6 as published. In Figure 6B, the integrated optical density ratio of p-p85/p85, p-Akt/Akt and p-mTOR/mTOR values do not correspond to the experiment group. The corrected Figure 6 and its caption appear below.

FIGURE 6
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Figure 6 IGF-1 is able to counteract the protective effect of PD-L1 knockdown by activating the PI3K/Akt/mTOR pathway. (A–G) Neutrophils from PD-L1WT/WT mice or PD-L1flox/flox mice stimulated with IFN-γ (10ng/ml) and LPS (1μg/ml) are treated with IGF-1 (10ng/ml) or DMSO for 21h. (A) IGF-1 can activate the PI3K/Akt/mTOR pathway confirmed by Protein levels of p85, p-p85, Akt, p-Akt, mTOR, p-mTOR in neutrophils. (B) Integrated optical density ratio of p-p85/p85, p-Akt/Akt, P-mTOR/mTOR. (C) Autophagy induction assessed with LC3B staining (confocal microscopy; green: LC3B; blue: DNA) in neutrophils (scale bar: 10um). (D) LC3B puncta/cell are depicted. (E) PD-L1, Beclin-1 and LC3B II/I immunoblotting in neutrophils. (F) Integrated optical density ratio of LC3B II/LC3B I.(G) MPO-DNA complex measured in NETs structures in neutrophils culture supernatant. The values presented are mean ± SEM (n=6; *P<0.05, one-way analysis of variance).

The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.

Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Keywords: ARDS, PD-L1, autophagy, neutrophils, neutrophil extracellular traps, anti-PD-L1 therapy

Citation: Zhu C-l, Xie J, Zhao Z-z, Li P, Liu Q, Guo Y, Meng Y, Wan X-j, Bian J-j, Deng X-m and Wang J-f (2022) Corrigendum: PD-L1 maintains neutrophil extracellular traps release by inhibiting neutrophil autophagy in endotoxin-induced lung injury. Front. Immunol. 13:1038083. doi: 10.3389/fimmu.2022.1038083

Received: 06 September 2022; Accepted: 22 September 2022;
Published: 06 October 2022.

Edited and Reviewed by:

Taruna Madan, National Institute for Research in Reproductive Health (ICMR), India

Copyright © 2022 Zhu, Xie, Zhao, Li, Liu, Guo, Meng, Wan, Bian, Deng and Wang. 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.

*Correspondence: Jia-feng Wang, amZ3YW5nQHNtbXUuZWR1LmNu; Xiao-ming Deng, ZGVuZ3BoZEBzbW11LmVkdS5jbg==; Jin-jun Bian, amluanVuYmljdUAxNjMuY29t

These authors have contributed equally to this work and share first authorship

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.