ArticlePLoS biology2019
Loss of adenomatous polyposis coli function renders intestinal epithelial cells resistant to the cytokine IL-22.
Article in PLoS biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- IL-22 increases proglucagon-expressing enteroendocrine cells via STAT3 in human iPSC-derived intestinal epithelium.Endocrinology · 2026Article
- The Role of Organoids in Advancing Colorectal Cancer Research: Insights and Future Directions.Cancers · 2025Review
- Vaccines for cancer interception in familial adenomatous polyposis.Frontiers in immunology · 2025Review
- Organoids as a tool to study homeostatic and pathological immune-epithelial interactions in the gut.Clinical and experimental immunology · 2024Review
- Oncostatin M-driven macrophage-fibroblast circuits as a drug target in autoimmune arthritis.Inflammation and regeneration · 2024Article
- Bi-directional signaling between the intestinal epithelium and type-3 innate lymphoid cells regulates secretory dynamics and interleukin-22.Mucosal immunology · 2024Article
- Cytokine-mediated crosstalk between cancer stem cells and their inflammatory niche from the colorectal precancerous adenoma stage to the cancerous stage: Mechanisms and clinical implications.Frontiers in immunology · 2022Review
- Loss of aryl hydrocarbon receptor suppresses the response of colonic epithelial cells to IL22 signaling by upregulating SOCS3.American journal of physiology. Gastrointestinal and liver physiology · 2022Article
- Acetaminophen-Induced Liver Injury Exposes Murine IL-22 as Sex-Related Gene Product.International journal of molecular sciences · 2021Article
- Mitochondrial Metabolism in the Intestinal Stem Cell Niche-Sensing and Signaling in Health and Disease.Frontiers in cell and developmental biology · 2020Review
- Research Progress of Intestinal Microecology in the Pathogenesis of Colorectal Adenoma and Carcinogenesis.Technology in cancer research & treatmentReview
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Interleukin-22 (IL-22) is a critical immune defence cytokine that maintains intestinal homeostasis and promotes wound healing and tissue regeneration, which can support the growth of colorectal tumours. Mutations in the adenomatous polyposis coli gene (Apc) are a major driver of familial colorectal cancers (CRCs). How IL-22 contributes to APC-mediated tumorigenesis is poorly understood. To investigate IL-22 signalling in wild-type (WT) and APC-mutant cells, we performed RNA sequencing (RNAseq) of IL-22-treated murine small intestinal epithelial organoids. In WT epithelia, antimicrobial defence and cellular stress response pathways were most strongly induced by IL-22. Surprisingly, although IL-22 activates signal transducer and activator of transcription 3 (STAT3) in APC-mutant cells, STAT3 target genes were not induced. Our analyses revealed that ApcMin/Min cells are resistant to IL-22 due to reduced expression of the IL-22 receptor, and increased expression of inhibitors of STAT3, particularly histone deacetylases (HDACs). We further show that IL-22 increases DNA damage and genomic instability, which can accelerate cellular transition from heterozygosity (ApcMin/+) to homozygosity (ApcMin/Min) to drive tumour formation. Our data reveal an unexpected role for IL-22 in promoting early tumorigenesis while excluding a function for IL-22 in transformed epithelial cells.
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Registered trials
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