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mTOR signaling mediates ILC3-driven immunopathology.

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Mammalian target of rapamycin (mTOR) complexes regulate innate lymphoid cells (ILCs). Both mTORC1 and mTORC2 control ILC numbers and inflammation, impacting gut immunity and disease.

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Area of Science:

  • Immunology
  • Cell Biology
  • Gastroenterology

Background:

  • Innate lymphoid cells (ILCs) play dual roles in mucosal immunity, offering protection but also contributing to immunopathology.
  • Mammalian target of rapamycin complex 1 (mTORC1) is known to influence ILC3 cytokine responses, but its role in IFN-γ-mediated pathology and the function of mTORC2 in ILC3s remain unclear.

Purpose of the Study:

  • To investigate the roles of mTORC1 and mTORC2 in the function and regulation of ILC3s.
  • To determine the impact of mTOR signaling on ILC3-driven immune responses and immunopathology in the gut.

Main Methods:

  • Utilized mice with specific defects in mTORC1 or mTORC2 within ILC3s.
  • Analyzed ILC3 maintenance, proliferation, cytokine production (IFN-γ), and inflammatory responses during experimental colitis.
  • Assessed the therapeutic effect of rapamycin treatment on colitis.

Main Results:

  • Both mTORC1 and mTORC2 are crucial for maintaining ILC3 populations in the small intestine at steady state.
  • Absence of mTOR signaling in ILC3s leads to reduced IFN-γ production upon activation.
  • Loss of mTORC1/mTORC2 in colonic ILC3s during colitis diminishes inflammatory mediators, neutrophil recruitment, and overall immunopathology.
  • Rapamycin treatment ameliorates disease severity during colitis.

Conclusions:

  • Both mTORC1 and mTORC2 signaling are critical for regulating ILC3 cell numbers and function.
  • mTOR signaling in ILC3s plays a significant role in controlling intestinal inflammation and immunopathology.
  • Targeting mTOR pathways may offer therapeutic potential for inflammatory conditions like colitis.