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Expansion of Interleukin-22-Producing Type 3 Innate Lymphoid Cells in the Gut of Tristetraprolin-Deficient Mice.

par De Toeuf, Bérengère ;Melchior, Maxime ;La, Caroline ;Villanueva Alcantara, Aresio ;Azouz, Abdulkader ;Martens, Vincent ;La, Celine ;Dubois, Ingrid ;Vande Velde, Sylvie ;Meyer, Lara ;Nguyen, Muriel ;Thomas, Séverine ;Libert, Frédérick ;Dumoutier, Laure LD;Blackshear, Perry J;Goriely, Stanislas
Référence European Journal of Immunology, 55, 4, page (e202350892)
Publication Publié, 2025-04-01

Article révisé par les pairs

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Résumé :

Tristetraprolin (TTP, encoded by Zfp36) is an RNA-binding protein that plays a major role in the control of inflammation. Zfp36-/- mice spontaneously develop a complex multiorgan inflammatory syndrome but no overt intestinal inflammation, suggesting the involvement of local regulatory mechanisms. In this study, we observed local expansion of IL-22-producing type 3 innate lymphoid cells (ILC3s) in the lamina propria of Zfp36-/- mice. Our findings demonstrate that this expansion was primarily influenced by cell-extrinsic cues. In the absence of IL-22, we observed delayed onset of arthritis in Zfp36-/- mice but no clear evidence of exacerbated intestinal inflammation under steady-state conditions. However, we show that Zfp36-/- mice were paradoxically protected from dextran sulfate sodium (DSS)-induced colitis and suggest that increased IL-22 production by ILC3 might contribute to this observation. Taken together, these data highlight the complex interplay between systemic inflammation and gut mucosal immune homeostasis.