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Inducible Operons: lac Operon

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The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
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Updated: Sep 18, 2025

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LKB1 regulates ILC3 postnatal development and effector function through metabolic programming.

Huasheng Zhang1,2,3, Linfeng Zhao1,2,3, Qingbing Zhang1,2,3

  • 1Center for Immune-Related Diseases at Shanghai Institute of Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Frontiers in Immunology
|June 20, 2025
PubMed
Summary
This summary is machine-generated.

Liver Kinase B1 (LKB1) is crucial for the development and function of Group 3 Innate Lymphoid Cells (ILC3s), which are vital for intestinal immunity. LKB1 deficiency impairs ILC3s, impacting gut homeostasis and host defense.

Keywords:
Liver Kinase B1 (LKB1)group 3 innate lymphoid cells (ILC3s)inflammationintestinal immune homeostasismetabolic programming

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Area of Science:

  • Immunology
  • Metabolism
  • Cell Biology

Background:

  • Group 3 Innate Lymphoid Cells (ILC3s) are critical for maintaining intestinal homeostasis and host defense.
  • Metabolic regulation significantly influences ILC3 activation and function.
  • The specific role of Liver Kinase B1 (LKB1), a key metabolic regulator, in ILC3 function and intestinal immunity is not well understood.

Purpose of the Study:

  • To investigate the role of LKB1 in intestinal ILC3s.
  • To determine how LKB1 affects ILC3 development, function, and metabolism.
  • To elucidate LKB1's contribution to intestinal immunity and host defense.

Main Methods:

  • Generated LKB1 conditional knockout mice using Rorccre and Stk11flox/flox strains.
  • Assessed ILC3 cell number and cytokine production via flow cytometry.
  • Utilized Citrobacter rodentium infection model and RT-qPCR, flow cytometry, and immunohistochemistry to evaluate intestinal defense and inflammatory responses.

Main Results:

  • LKB1 is essential for ILC3 postnatal development, with LKB1-deficient mice showing reduced ILC3 numbers.
  • Ablation of LKB1 in ILC3s diminished IL-22 production and compromised protection against Citrobacter rodentium infection.
  • LKB1 deficiency impaired ILC3 metabolism, evidenced by reduced glycolysis, oxidative phosphorylation, and mitochondrial mass.

Conclusions:

  • LKB1 is a key regulator of intestinal ILC3 development and effector function.
  • LKB1 links metabolic control to intestinal immune homeostasis.
  • These findings highlight LKB1's importance in maintaining gut health and suggest potential therapeutic avenues.