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Related Experiment Video

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From model to man: Understanding Tregs' dual role in MASLD.

Janine Dywicki1, Laura Elisa Buitrago-Molina1, Anna K Baumann1

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Metabolic dysfunction-associated steatotic liver disease (MASLD) can progress to MASH without adaptive immunity. Increased regulatory T cells (Tregs) correlated with worse MASH, suggesting a pro-inflammatory role for IL-17-producing Tregs.

Keywords:
Adaptive immunityClonal T cell expansionFoxp3ImmunometabolismKupffer cellsMASHMonocyte-derived macrophagesRegulatory T cellsT-cell receptor repertoire

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Area of Science:

  • Immunology
  • Hepatology
  • Metabolic Diseases

Background:

  • Metabolic Dysfunction-associated Steatotic Liver Disease (MASLD) affects 30% of the global population, often linked to obesity and diabetes.
  • A subset of MASLD progresses to Metabolic Dysfunction-associated Steatohepatitis (MASH), increasing liver cancer risk.
  • The role of intrahepatic immune cells, particularly regulatory T cells (Tregs), in MASH pathogenesis is not fully understood.

Purpose of the Study:

  • To investigate the impact of adaptive immunity on the development and progression of MASH.
  • To elucidate the specific role of regulatory T cells (Tregs) in MASH pathogenesis.
  • To identify potential immunomodulatory therapeutic targets for MASH.

Main Methods:

  • Utilized a high-fat/high-carbohydrate diet (HF-HCD) mouse model (wild-type and Rag2-deficient) to induce MASH.
  • Analyzed intrahepatic immune cell populations, including Tregs and T effector cells (Teff).
  • Correlated immune cell profiles with liver pathology and metabolic parameters, supplemented with human liver samples.

Main Results:

  • HF-HCD induced MASH and glucose intolerance independently of adaptive immunity.
  • Increased intrahepatic Treg numbers and Treg/Teff ratio were observed, correlating with increased MASH severity.
  • A subset of Tregs expressed IL-17 (TH17-skewed), and this correlated with more severe liver pathology.

Conclusions:

  • Adaptive immunity is not essential for initiating diet-induced MASH but can amplify liver injury.
  • Expansion of Tregs, particularly IL-17-producing Tregs, is associated with increased MASH severity, not protection.
  • Findings suggest stage-specific immunomodulatory strategies, potentially targeting pro-inflammatory T cell subsets, could complement metabolic therapies for MASH.