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CORRECTION article

Front. Immunol., 02 January 2026

Sec. Molecular Innate Immunity

Volume 16 - 2025 | https://doi.org/10.3389/fimmu.2025.1761117

Correction: Neutrophils as key drivers of pulmonary fibrosis: unveiling mechanisms and therapeutic implications

This article is a correction to:

  1. Neutrophils as key drivers of pulmonary fibrosis: unveiling mechanisms and therapeutic implications

    1. Read original article
Xiuping Liang&#x;Xiuping Liang1†Yanhong Li&#x;Yanhong Li1†Ziyi TangZiyi Tang1Yubin Luo*Yubin Luo1*Yi Liu,*Yi Liu1,2*
  • 1Department of Rheumatology & Immunology, Laboratory of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, Sichuan, China
  • 2West China Lecheng Hospital, Sichuan University, Boao, Hainan, China

A Correction on
Neutrophils as key drivers of pulmonary fibrosis: unveiling mechanisms and therapeutic implications

By Liang X, Li Y, Tang Z, Luo Y and Liu Y (2025) Front. Immunol. 16:1718092. doi: 10.3389/fimmu.2025.1718092

There was a mistake in Figure 1 and Figure 2 as published. The content of Figure 1 and Figure 2 were erroneously switched. The corrected Figure 1 and Figure 2 appears below.

Figure 1
Diagram illustrating the roles of neutrophils in lung fibrosis, divided into three stages: recruitment, activation, and fibrosis. Each stage represents cellular interactions involving neutrophils, macrophages, T cells, B cells, epithelial cells, fibroblasts, and others. Symbols for NETosis, cytokines, chemokines, platelets, and apoptosis cells are included, showing progression from recruitment to activation and ultimately fibrosis, with myofibroblast formation. Accompanied by a key describing each cell type and process.

Figure 1. Diagram illustrating the roles of neutrophils in lung fibrosis across three stages: recruitment, activation, and fibrosis.

Figure 2
Diagram illustrating neutrophil-centric crosstalk in lung fibrosis, showing recruitment, activation, and pro-fibrosis processes involving interactions with platelets, macrophages, T cells, and B cells. It depicts molecular signals like cytokines and chemokines and outcomes like apoptosis, epithelial-mesenchymal transition (EMT), fibroblast-to-myofibroblast transition (FMT), and cell proliferation in lung epithelial and fibroblast cells.

Figure 2. Neutrophil-centric crosstalk in lung fibrosis. The fibrotic process involves coordinated cellular interactions: (1) Macrophages, T cells, B cells and platelets recruit and activate neutrophils; (2) Activated neutrophils release NETs, NE, IL-1β, and TNF-α; (3) These effector molecules target lung epithelial and fibroblast cells, promoting apoptosis, EMT, and FMT to drive fibrosis. CXCL2, C-X-C motif chemokine ligand 2; VIP, vasoactive intestinal peptide; TGF-β1, transforming growth factor beta 1; IL-18, interleukin-18; IL-1β, interleukin-1 beta; C5a, complement component 5a; C5aR1, complement C5a receptor 1; GPV, glycoprotein V; CD40L, CD40 ligand; BAFF, B cell activating factor; IL-17A, interleukin-17A; NETosis, neutrophil extracellular trap formation; DNA, deoxyribonucleic acid; TNF-α, tumor necrosis factor alpha; IL-1β, interleukin-1 beta; MPO, myeloperoxidase; NE, neutrophil elastase; EMT, epithelial-mesenchymal transition; FMT, fibroblast-myofibroblasttransition.

The original version of this 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: pulmonary fibrosis, neutrophils, neutrophil extracellular traps, neutrophil elastase, crosstalk

Citation: Liang X, Li Y, Tang Z, Luo Y and Liu Y (2026) Correction: Neutrophils as key drivers of pulmonary fibrosis: unveiling mechanisms and therapeutic implications. Front. Immunol. 16:1761117. doi: 10.3389/fimmu.2025.1761117

Received: 05 December 2025; Accepted: 15 December 2025; Revised: 09 December 2025;
Published: 02 January 2026.

Edited and reviewed by:

Yuan Liu, Chinese Academy of Sciences, China

Copyright © 2026 Liang, Li, Tang, Luo and Liu. 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: Yubin Luo, bHVveXViaW4yMDE2QDE2My5jb20=; Yi Liu, eWlsaXU4OTk5QHdjaHNjdS5jbg==

†These authors have contributed equally to this work

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.