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Microbiota-induced tissue signals regulate ILC3-mediated antigen presentation.

Frank Michael Lehmann1, Nicole von Burg1,2, Robert Ivanek3,4

  • 1Department of Biomedicine and University Children's Hospital of Basel, University of Basel, 4058, Basel, Switzerland.

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|April 15, 2020
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Group 3 innate lymphoid cells (ILC3s) in the gut down-modulate MHC II antigen presentation, unlike in the spleen. Microbiota-induced IL-23 signaling silences MHC II in ILC3s, impacting T cell responses.

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Area of Science:

  • Immunology
  • Cell Biology
  • Microbiome Research

Background:

  • Group 3 innate lymphoid cells (ILC3s) are crucial for immune responses but exhibit tissue-specific differences in T cell interaction.
  • The mechanisms regulating ILC3 function and T cell priming in the gut remain poorly understood.

Purpose of the Study:

  • To investigate the signals controlling ILC3-mediated T cell responses in the intestinal mucosa.
  • To elucidate the molecular pathways underlying tissue-specific regulation of ILC3s.

Main Methods:

  • Analysis of MHC II expression in intestinal versus splenic ILC3s.
  • Investigating the role of IL-23 signaling in regulating MHC II expression via mTORC1 and STAT3 pathways.
  • Assessing the impact of interferon-γ on ILC3 function in splenic contexts.

Main Results:

  • Intestinal natural cytotoxicity receptor-negative (NCR-) ILC3s show down-modulated MHC II antigen presentation transcripts compared to splenic ILC3s.
  • Microbiota-induced IL-23 signaling reversibly silences MHC II expression in intestinal ILC3s, dependent on mTORC1 and STAT3 phosphorylation.
  • Splenic interferon-γ induces MHC II expression and promotes CD4+ T cell stimulation by ILC3s.

Conclusions:

  • IL-23 signaling acts as a key regulator of MHC II expression in intestinal ILC3s, thereby controlling their capacity to present antigens to T cells.
  • These findings reveal distinct biological circuits governing tissue-specific ILC3-T cell interactions, with potential implications for immune-related diseases.