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Immune surveillance

Excess lipids on endosomes dictate NLRP3 localization and inflammasome activation

Diverse inflammasome stimuli recruit NLRP3 to dysfunctional endosomes via interactions with lipids that accumulate in excess on these organelles. Excess lipid detection may be a common principle that explains NLRP3 function in health and disease.

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Fig. 1: Recruitment of NLRP3 to excess lipids on dysfunctional endosomes ensures efficient inflammasome activities.

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Acknowledgements

This work was supported by National Institutes of Health (NIH) grants AI133524, AI093589, AI116550 and P30DK34854.

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Correspondence to Jonathan C. Kagan.

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Competing interests

J.C.K. consults and holds equity in Corner Therapeutics, Larkspur Biosciences and Neumora Therapeutics. None of these relationships influenced this work.

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Kagan, J.C. Excess lipids on endosomes dictate NLRP3 localization and inflammasome activation. Nat Immunol 24, 3–4 (2023). https://doi.org/10.1038/s41590-022-01364-2

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