ILC1 as critical gatekeepers in autoimmune kidney damage.

A recent article has shown that blocking NKp46 signaling reduces injury, highlighting these cells as key drivers of organ damage and potential therapeutic targets in autoimmune diseases. In lupus nephritis, NKp46+ ILC1s orchestrate kidney inflammation by producing CSF2, driving the expansion of pro-inflammatory macrophages that infiltrate epithelial niches and exacerbate tissue damage.