Triggering Receptor Expressed on Myeloid Cells‐2 Regulates Innate Lymphoid Cell Levels in Bleomycin‐Induced Pulmonary Fibrosis
4 affiliations
- 1Department of Chest Medicine Taipei Veterans General Hospital Taipei Taiwan
- 2Institute of Microbiology and Immunology School of Life Sciences, National Yang Ming Chiao Tung University Taipei Taiwan
- 3School of Medicine, National Yang Ming Chiao Tung University Taipei Taiwan
- 4Taipei Hospital, Ministry of Health and Welfare Taipei Taiwan
Abstract
Idiopathic pulmonary fibrosis, a pathological change causing poor outcomes, is not reversible despite current antifibrotic therapy. Emerging evidence suggests that innate lymphoid cells (ILCs) mediate lung inflammation and fibrosis after stimulation by endogenous factors. Triggering receptor expressed on myeloid cells‐2 (TREM2) is known to regulate inflammation in various diseases. However, the relationship between TREM2 and ILCs in pulmonary fibrosis is unclear. This study aimed to explore the role of TREM2 in regulating ILC activation in bleomycin (BLM)‐induced pulmonary fibrosis. We first examined the role of TREM2 in regulating ILC expression in a mouse model of BLM‐induced pulmonary fibrosis, and subsequently assessed the levels of ILCs, pulmonary fibrosis, and inflammation using histological staining and molecular biology techniques. These results were compared between wild‐type (WT) and TREM2 knockout (KO) mice. Compared with those in WT mice, inflammatory cell aggregation and collagen fiber deposition were more prominent in TREM2‐KO mice after intratracheal BLM injection. Compared with those in WT mice, there was a pronounced increase in GATA3 and RORγt expression in lung tissues from TREM2‐KO mice. In adaptive transfer experiments, ILC‐enriched population isolated from WT mice after BLM stimulation in vivo increased the expression of TGF‐β, α‐SMA, and collagen‐1 in naïve WT mice. Immunofluorescence staining revealed GATA3 expression in the lung tissues of TREM2‐KO mice after BLM stimulation. Compared with those receiving ILCs from WT mice, those receiving adoptive transfer of ILC‐enriched population from TREM2‐KO mice exhibited more lung injury and fibrosis. In conclusion, TREM2 decreases ILC activity to reduce BLM‐induced pulmonary fibrosis.
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BibTeX
@article{shen2026triggering,
title = {{Triggering Receptor Expressed on Myeloid Cells‐2 Regulates Innate Lymphoid Cell Levels in Bleomycin‐Induced Pulmonary Fibrosis}},
author = {Hsiao‐Chin Shen and Nien‐Jung Chen and Chuan‐Yen Sun and Wen‐Kuang Yu and Vincent Yi‐Fong Su and Wan‐Ling Yang and Wei‐Chih Chen and Kuang‐Yao Yang},
journal = {Kaohsiung Journal of Medical Sciences},
year = {2026},
month = nov,
doi = {10.1002/kjm2.70209},
url = {https://doi.org/10.1002/kjm2.70209},
note = {CC BY},
}
RIS
TY - JOUR
TI - Triggering Receptor Expressed on Myeloid Cells‐2 Regulates Innate Lymphoid Cell Levels in Bleomycin‐Induced Pulmonary Fibrosis
AU - Hsiao‐Chin Shen
AU - Nien‐Jung Chen
AU - Chuan‐Yen Sun
AU - Wen‐Kuang Yu
AU - Vincent Yi‐Fong Su
AU - Wan‐Ling Yang
AU - Wei‐Chih Chen
AU - Kuang‐Yao Yang
PY - 2026
DA - 2026/11/06
JO - Kaohsiung Journal of Medical Sciences
DO - 10.1002/kjm2.70209
UR - https://doi.org/10.1002/kjm2.70209
AB - Idiopathic pulmonary fibrosis, a pathological change causing poor outcomes, is not reversible despite current antifibrotic therapy. Emerging evidence suggests that innate lymphoid cells (ILCs) mediate lung inflammation and fibrosis after stimulation by endogenous factors. Triggering receptor expressed on myeloid cells‐2 (TREM2) is known to regulate inflammation in various diseases. However, the relationship between TREM2 and ILCs in pulmonary fibrosis is unclear. This study aimed to explore the role of TREM2 in regulating ILC activation in bleomycin (BLM)‐induced pulmonary fibrosis. We first examined the role of TREM2 in regulating ILC expression in a mouse model of BLM‐induced pulmonary fibrosis, and subsequently assessed the levels of ILCs, pulmonary fibrosis, and inflammation using histological staining and molecular biology techniques. These results were compared between wild‐type (WT) and TREM2 knockout (KO) mice. Compared with those in WT mice, inflammatory cell aggregation and collagen fiber deposition were more prominent in TREM2‐KO mice after intratracheal BLM injection. Compared with those in WT mice, there was a pronounced increase in GATA3 and RORγt expression in lung tissues from TREM2‐KO mice. In adaptive transfer experiments, ILC‐enriched population isolated from WT mice after BLM stimulation in vivo increased the expression of TGF‐β, α‐SMA, and collagen‐1 in naïve WT mice. Immunofluorescence staining revealed GATA3 expression in the lung tissues of TREM2‐KO mice after BLM stimulation. Compared with those receiving ILCs from WT mice, those receiving adoptive transfer of ILC‐enriched population from TREM2‐KO mice exhibited more lung injury and fibrosis. In conclusion, TREM2 decreases ILC activity to reduce BLM‐induced pulmonary fibrosis.
SN - 2410-8650
SN - 1607-551X
ER -