Natural Killer Cell TGF-β Signaling Regulates Postnatal Lung Development.

NK cell–specific loss of TGF-β receptor signaling in neonatal mice (Tgfbr2 NK-/-) reduces distal arteriolar density and impairs alveolarization, with sex-specific long-term lung function deficits.

• Why it matters: Bronchopulmonary dysplasia involves impaired vascularization, dysregulated TGF-β signaling, and senescent cell accumulation, but how NK cell TGF-β signaling shapes postnatal lung patterning is unclear.
• What they did: The study used Tgfbr2 NK-/- mice to assess lung structure, NK infiltration, senescence markers, and lung function across neonatal and adult time points, plus single-cell RNA sequencing in mice and human BPD samples.
• The result: TGF-β-insensitive NK cells showed excessive clearance of senescent endothelial cells, enhancing a BPD-like phenotype in naïve Tgfbr2 NK-/- mice yet protecting under hyperoxia; HCW9218 prevented senescent cell accumulation and rescued hyperoxia lung development.

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