Interferon regulatory factor 1 (IRF-1) promotes intestinal group 3 innate lymphoid responses during Citrobacter rodentium infection

Angelika Schmalzl, Tamara Leupold, Lucas Kreiss, Maximilian Waldner, Sebastian Schürmann, Markus F. Neurath, Christoph Becker and Stefan Wirtz ()
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Angelika Schmalzl: Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg
Tamara Leupold: Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg
Lucas Kreiss: Friedrich-Alexander University Erlangen-Nürnberg
Maximilian Waldner: Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg
Sebastian Schürmann: Friedrich-Alexander University Erlangen-Nürnberg
Markus F. Neurath: Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg
Christoph Becker: Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg
Stefan Wirtz: Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg

Nature Communications, 2022, vol. 13, issue 1, 1-15

Abstract: Abstract Group 3 innate lymphoid cells (ILC3s) are crucial mediators of immunity and epithelial barrier function during immune responses against extracellular bacteria. Here, we identify Interferon regulatory factor 1 (IRF-1), a transcription factor previously associated with type 1 immunity, as an essential regulator of intestinal ILC3 accumulation and effector cytokine production. We demonstrate that IRF-1 is upregulated in the context of infection with the enteropathogen Citrobacter rodentium and that its presence is central for anatomical containment and prevention of pathogen dissemination. We furthermore show that IRF-1 is required in order for intestinal ILC3s to produce large amounts of the protective effector cytokine IL-22 early in the course of infection. On a molecular level, our data indicate that IRF-1 controls ILC3 numbers and their activation by direct transcriptional regulation of the IL-12Rβ1 chain, thereby allowing ILCs to physiologically respond to IL-23 stimulation.

Date: 2022
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DOI: 10.1038/s41467-022-33326-5

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