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LKB1 regulates ILC3 postnatal development and effector function through metabolic programming

GSE284792 Mus musculus Expression profiling by high throughput sequencing 4 samples Submitted 2025/06/25 Platform GPL34290
Summary
Group 3 Innate Lymphoid Cells (ILC3s) is important for maintaining intestinal homeostasis and host defense. Emerging studies have shown that metabolic regulation plays a crucial role in regulating ILC3 activation and function. However, the role of Liver Kinase B1 (LKB1), key metabolic regulator, in regulating ILC3 function and intestinal immunity remains poorly understood. In this study, we show that LKB1 is essential for ILC3 postnatal development, effector function, and intestinal immunity. Ablation of LKB1 in ILC3s results in reduced cell number due to increased apoptosis and reduced proliferation, which occurs at 2 -3 weeks after birth. In addition, LKB1 deletion leads to diminished IL-22 production and less protection against C.rodentium infection. Mechanistically, LKB1 deficiency led to impaired mitochondrial metabolism, as indicated by reduced glycolysis and oxidative phosphorylation and less mitochondrial mass. Together, our data demonstrate that LKB1 promotes ILC3 postnatal development and effector function to maintain intestinal immune homeostasis.
Published in
LKB1 regulates ILC3 postnatal development and effector function through metabolic programming
Zhang H, Zhao L, Zhang Q et al. · Frontiers in immunology 2025 · PMID 40539052 · doi:10.3389/fimmu.2025.1587256
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Also filed as BioProject PRJNA1200661 and SRA study SRP552734. Searching any of these in the dataset finder brings you back here.

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