ILC1 as critical gatekeepers in autoimmune kidney damage
- PMID: 39642908
- DOI: 10.1111/imcb.12842
ILC1 as critical gatekeepers in autoimmune kidney damage
Abstract
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.
Keywords: inflammation; innate lymphoid cells; systemic lupus erythematosus (SLE).
© 2024 the Australian and New Zealand Society for Immunology, Inc.
Comment on
-
Amplification of autoimmune organ damage by NKp46-activated ILC1s.Nature. 2024 Oct;634(8035):952-960. doi: 10.1038/s41586-024-07907-x. Epub 2024 Aug 13. Nature. 2024. PMID: 39137897
References
REFERENCES
-
- Biniaris‐Georgallis SI, Aschman T, Stergioula K, et al. Amplification of autoimmune organ damage by NKp46‐activated ILC1s. Nature 2024; 634: 952–960.
-
- Tang PM, Nikolic‐Paterson DJ, Lan HY. Macrophages: versatile players in renal inflammation and fibrosis. Nat Rev Nephrol 2019; 15: 144–158.
-
- Guo C, Zhou M, Zhao S, et al. Innate lymphoid cell disturbance with increase in ILC1 in systemic lupus erythematosus. Clin Immunol 2019; 202: 49–58.
-
- Narni‐Mancinelli E, Gauthier L, Baratin M, et al. Complement factor P is a ligand for the natural killer cell‐activating receptor NKp46. Sci Immunol 2017; 2: eaam9628.
-
- Vivier E, Artis D, Colonna M, et al. Innate lymphoid cells: 10 years on. Cell 2018; 174: 1054–1066.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
