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The interleukin 22–oncostatin M axis promotes intestinal inflammation and tumorigenesis [Epithelial_cells_BulkRNA-seq]

GSE269505 Mus musculus Expression profiling by high throughput sequencing 9 samples Submitted 2025/03/27 Platform GPL33944
Summary
Multicellular cytokine networks regulate the onset of intestinal inflammation and colitis-associated cancer (CAC). Interleukin 22 (IL-22) promotes epithelial cell recovery but can also drive inflammation and tumorigenesis. We demonstrate that IL-22 from innate lymphoid cells activates STAT3 and increases OSM receptor expression in intestinal epithelial cells. This activation leads to sustained STAT3 activity via OSM, promoting inflammation and tumorigenesis. Deleting the OSM receptor or blocking OSM pharmacologically mitigates colitis and CAC. Our findings highlight the IL-22-OSM axis as a potential therapeutic target for these conditions.
Published in
The IL-22-oncostatin M axis promotes intestinal inflammation and tumorigenesis
Cineus R, Luo Y, Saliutina M et al. · Nature immunology 2025 · PMID 40447860 · doi:10.1038/s41590-025-02149-z
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Also filed as BioProject PRJNA1122160 and SRA study SRP512979. Searching any of these in the dataset finder brings you back here.

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