ILC1作为自身免疫性肾损伤的关键守门人。
ILC1 as critical gatekeepers in autoimmune kidney damage.
作者信息
Seillet Cyril, Xiong Le
机构信息
The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia.
Department of Medical Biology, University of Melbourne, Parkville, VIC, Australia.
出版信息
Immunol Cell Biol. 2025 Jan;103(1):9-11. doi: 10.1111/imcb.12842. Epub 2024 Dec 6.
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.
最近的一篇文章表明，阻断NKp46信号传导可减轻损伤，突出了这些细胞作为自身免疫性疾病中器官损伤的关键驱动因素和潜在治疗靶点的作用。在狼疮性肾炎中，NKp46 ILC1s通过产生CSF2来协调肾脏炎症，促使促炎性巨噬细胞扩增，这些巨噬细胞浸润上皮龛并加剧组织损伤。
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