Type I IFN promotes ILC2-to-ILC1 plasticity in pre-clinical radiation-induced lung injury.

Type I interferon promotes ILC2-to-ILC1 plasticity, contributing to radiation-induced lung injury in a mouse model.

• Why it matters: Understanding immune mechanisms in RILI is crucial because it is a common toxicity limiting radiotherapy effectiveness for lung cancer, yet these mechanisms are poorly understood.
• What they did: Researchers used a mouse model with high-dose lung irradiation, combined with flow cytometry, cytokine profiling, and single-cell RNA sequencing, to analyze ILC populations and the role of type I IFN.
• The result: Findings show that type I IFN induces ILC2-to-ILC1 plasticity, and inhibiting this signaling reduces lung damage, suggesting a potential therapeutic target for RILI.