Triggering Receptor Expressed on Myeloid Cells-2 Regulates Innate Lymphoid Cell Levels in Bleomycin-Induced Pulmonary
Hsiao-Chin Shen1,2,3,4, Nien-Jung Chen2, Chuan-Yen Sun1,3
1Department of Chest Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
The Kaohsiung Journal of Medical Sciences
|April 3, 2026
Summary
Triggering receptor expressed on myeloid cells-2 (TREM2) reduces innate lymphoid cell (ILC) activity, thereby decreasing pulmonary fibrosis in a mouse model. This finding offers new insights into idiopathic pulmonary fibrosis treatment.
Area of Science:
- Immunology
- Pulmonary Medicine
- Cell Biology
Background:
- Idiopathic pulmonary fibrosis is irreversible and associated with poor outcomes.
- Innate lymphoid cells (ILCs) are implicated in lung inflammation and fibrosis.
- The role of Triggering receptor expressed on myeloid cells-2 (TREM2) in pulmonary fibrosis and its interaction with ILCs remain unclear.
Purpose of the Study:
- To investigate the role of TREM2 in regulating ILC activation in bleomycin (BLM)-induced pulmonary fibrosis.
- To compare pulmonary fibrosis and inflammation levels between wild-type (WT) and TREM2 knockout (KO) mice.
Main Methods:
- Utilized a mouse model of BLM-induced pulmonary fibrosis.
- Assessed ILC levels, pulmonary fibrosis, and inflammation via histological staining and molecular biology.
- Conducted adaptive transfer experiments with ILC-enriched populations.
Main Results:
- TREM2-KO mice showed increased inflammatory cell aggregation and collagen deposition post-BLM exposure compared to WT mice.
- GATA3 and RORγt expression were significantly elevated in TREM2-KO mice's lung tissues.
- Adoptive transfer of ILCs from TREM2-KO mice exacerbated lung injury and fibrosis in recipient mice.
Conclusions:
- TREM2 plays a protective role by suppressing ILC activity in BLM-induced pulmonary fibrosis.
- Targeting TREM2 may offer a novel therapeutic strategy for pulmonary fibrosis.
