Front. Immunol. Frontiers in Immunology Front. Immunol. 1664-3224 Frontiers Media S.A. 10.3389/fimmu.2025.1761117 Correction Correction: Neutrophils as key drivers of pulmonary fibrosis: unveiling mechanisms and therapeutic implications LiangXiuping 1 † Conceptualization Data curation Formal analysis Funding acquisition Investigation Methodology Project administration Resources Software Supervision Validation Visualization Writing – original draft Writing – review & editing LiYanhong 1 † Conceptualization Data curation Formal analysis Investigation Methodology Project administration Resources Software Supervision Validation Visualization Writing – original draft Writing – review & editing TangZiyi 1 Conceptualization Data curation Formal analysis Investigation Methodology Project administration Resources Software Supervision Validation Visualization Writing – original draft Writing – review & editing LuoYubin 1 * Conceptualization Data curation Formal analysis Investigation Methodology Project administration Resources Software Supervision Validation Visualization Writing – original draft Writing – review & editing LiuYi 1 2 * Conceptualization Data curation Formal analysis Funding acquisition Investigation Methodology Project administration Resources Software Supervision Validation Visualization Writing – original draft Writing – review & editing Department of Rheumatology & Immunology, Laboratory of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, Sichuan, China West China Lecheng Hospital, Sichuan University, Boao, Hainan, China Correspondence: Yubin Luo, luoyubin2016@163.com; Yi Liu, yiliu8999@wchscu.cn

These authors have contributed equally to this work

 02 01 2026 2025 16 1761117 05 12 2025 15 12 2025 09 12 2025 Copyright © 2026 Liang, Li, Tang, Luo and Liu. 2026 Liang, Li, Tang, Luo and Liu https://creativecommons.org/licenses/by/4.0/ 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. 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 pulmonary fibrosis neutrophils neutrophil extracellular traps neutrophil elastase crosstalk section-at-acceptance Molecular Innate Immunity

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.

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

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.

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.

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.

The original version of this article has been updated.

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Edited and reviewed by: Yuan Liu, Chinese Academy of Sciences, China