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BACH2 controls ILC3 function via PPARγ-dependent mitochondrial metabolism.

Jianye Wang1,2, Ying Wang1, Gaoyu Liu1,2

  • 1Department of Immunology, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), State Key Laboratory of Experimental Hematology, Tianjin Institute of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.

The Journal of Experimental Medicine
|April 28, 2026
PubMed
Summary
This summary is machine-generated.

The transcription factor BACH2 (BTB domain and CNC homolog 2) regulates group 3 innate lymphoid cells (ILC3s) crucial for gut immunity. Loss of BACH2 worsens inflammatory bowel disease (IBD) models, but its activation via PPARγ protects against colitis.

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Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Group 3 innate lymphoid cells (ILC3s) are vital for intestinal barrier immunity.
  • Dysfunctional ILC3s are implicated in inflammatory bowel disease (IBD) pathogenesis.
  • Mechanisms regulating ILC3 function are not fully understood.

Purpose of the Study:

  • To investigate the role of the transcription factor BACH2 in regulating intestinal ILC3s.
  • To elucidate the molecular mechanisms by which BACH2 controls ILC3 function.
  • To explore therapeutic potential of targeting BACH2-PPARγ signaling in IBD.

Main Methods:

  • Analysis of BACH2 expression in ILC3s from IBD patients and healthy donors.
  • Conditional ablation of BACH2 in ILC3s in a murine colitis model.
  • Assessment of mitochondrial oxidative phosphorylation and PPARγ activity.
  • Pharmacological activation of PPARγ using rosiglitazone.

Main Results:

  • Reduced BACH2 expression observed in ILC3s from IBD patients.
  • BACH2 deficiency in ILC3s impaired cell function and exacerbated colitis severity.
  • BACH2 promotes ILC3 function by enhancing mitochondrial oxidative phosphorylation via PPARγ.
  • PPARγ is a direct transcriptional target of BACH2.
  • Rosiglitazone treatment restored ILC3 function and ameliorated colitis in BACH2-deficient mice.

Conclusions:

  • BACH2 is a critical regulator of intestinal ILC3 function.
  • The BACH2-PPARγ signaling pathway protects against colitis.
  • Targeting this pathway offers a potential therapeutic strategy for IBD.