Nature Immunology, Published online: 25 July 2025; doi:10.1038/s41590-025-02217-4

Sajti and colleagues identify TREM2 as a critical factor in myeloid cells in response to hyperoxia-induced lung injury in neonates, finding that TREM2 deficiency protects mice from bronchopulmonary dysplasia.



Summary

A recent Nature Immunology study reveals that TREM2, a protein found in myeloid cells, plays a key role in hyperoxia-induced lung injury in newborn mice, a condition often leading to bronchopulmonary dysplasia (BPD). Sajti and colleagues discovered that mice lacking TREM2 were protected from developing BPD when exposed to high oxygen levels. This suggests that TREM2 exacerbates lung injury in neonates exposed to hyperoxia, potentially making it a promising therapeutic target for preventing or treating BPD.

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