Microbiota-induced tissue signals regulate ILC3-mediated antigen presentation

Frank Michael Lehmann, Nicole von Burg, Robert Ivanek, Claudia Teufel, Edit Horvath, Annick Peter, Gleb Turchinovich, Daniel Staehli, Tobias Eichlisberger, Mercedes Gomez de Agüero, Mairene Coto-Llerena, Michaela Prchal-Murphy, Veronika Sexl, Mohamed Bentires-Alj, Christoph Mueller and Daniela Finke ()
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Frank Michael Lehmann: University of Basel
Nicole von Burg: University of Basel
Robert Ivanek: University of Basel
Claudia Teufel: University of Basel
Edit Horvath: University of Basel
Annick Peter: University of Basel
Gleb Turchinovich: University of Basel
Daniel Staehli: University of Basel
Tobias Eichlisberger: Friedrich Miescher Institute for Biomedical Research
Mercedes Gomez de Agüero: University of Bern
Mairene Coto-Llerena: University of Basel
Michaela Prchal-Murphy: University of Veterinary Medicine Vienna
Veronika Sexl: University of Veterinary Medicine Vienna
Mohamed Bentires-Alj: University of Basel
Christoph Mueller: University of Bern
Daniela Finke: University of Basel

Nature Communications, 2020, vol. 11, issue 1, 1-15

Abstract: Abstract Although group 3 innate lymphoid cells (ILC3s) are efficient inducers of T cell responses in the spleen, they fail to induce CD4+ T cell proliferation in the gut. The signals regulating ILC3-T cell responses remain unknown. Here, we show that transcripts associated with MHC II antigen presentation are down-modulated in intestinal natural cytotoxicity receptor (NCR)− ILC3s. Further data implicate microbiota-induced IL-23 as a crucial signal for reversible silencing of MHC II in ILC3s, thereby reducing the capacity of ILC3s to present antigen to T cells in the intestinal mucosa. Moreover, IL-23-mediated MHC II suppression is dependent on mTORC1 and STAT3 phosphorylation in NCR− ILC3s. By contrast, splenic interferon-γ induces MHC II expression and CD4+ T cell stimulation by NCR− ILC3s. Our results thus identify biological circuits for tissue-specific regulation of ILC3-dependent T cell responses. These pathways may have implications for inducing or silencing T cell responses in human diseases.

Date: 2020
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DOI: 10.1038/s41467-020-15612-2

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