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‐...

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Bibliographic Details
Published in:Immunology and cell biology 2024-12, Vol.103 (1), p.9-11
Main Authors: Seillet, Cyril, Xiong, Le
Format: Article
Language:English
Subjects:
Autoimmune diseases
inflammation
innate lymphoid cells
Kidneys
Lupus nephritis
Macrophages
systemic lupus erythematosus (SLE)
Therapeutic targets
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Summary: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.
ISSN:0818-9641
1440-1711
1440-1711
DOI:10.1111/imcb.12842