ArticleMucosal immunology2014
IL-23R+ innate lymphoid cells induce colitis via interleukin-22-dependent mechanism.
Article in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers.
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Who cites it
132 citing papers in PubMed, 200 citations in OpenAlex.
- Review
- Pediococcus pentosaceus JNL0053 Mitigates DSS-induced Colitis in Mice Via the IL-22-Gut Barrier Pathway.Probiotics and antimicrobial proteins · 2026Article
- DNA From Neutrophil Extracellular Traps Restricts Group 3 Innate Lymphoid Cells Function in Intestinal Epithelial Repair via CCDC25.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Review
- Phantom of the immunologic opera: Unmasking the role of innate lymphoid cells (ILC) in inborn errors of immunity (IEI).Journal of human immunity · 2025Review
- The interaction network between group 3 innate lymphoid cells and other cells.Fundamental research · 2025Review
- Targeting the IL-23 Receptor Gene: A Promising Approach in Inflammatory Bowel Disease Treatment.International journal of molecular sciences · 2025Review
- MicroRNA-142 regulates gut associated lymphoid tissues and group 3 innate lymphoid cells.Mucosal immunology · 2025Article
- Novel Insights into the Pathogenesis of Inflammatory Bowel Diseases.Biomedicines · 2025Review
- Fundamental and emerging insights into innate and adaptive immunity in inflammatory bowel diseases.Frontiers in immunology · 2025Review
- I don't know about you, but I'm feeling IL-22.Cytokine & growth factor reviews · 2024Review
- IL-22, a vital cytokine in autoimmune diseases.Clinical and experimental immunology · 2024Review
- Eosinophils mitigate intestinal fibrosis while promoting inflammation in a chronic DSS colitis model and co-culture model with fibroblasts.Scientific reports · 2024Article
- Type 17 immunity: novel insights into intestinal homeostasis and autoimmune pathogenesis driven by gut-primed T cells.Cellular & molecular immunology · 2024Review
- Human IL-22 receptor-targeted small protein antagonist suppress murine DSS-induced colitis.Cell communication and signaling : CCS · 2024Article
- The mode of action of IL-23 in experimental inflammatory arthritic pain and disease.Arthritis research & therapy · 2024Article
- IL-22 regulates MASTL expression in intestinal epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- OLFM4 modulates intestinal inflammation by promoting IL-22Communications biology · 2024Article
- IL-22 promotes mucin-type O-glycosylation and MATH1Cell reports · 2024Article
- Association between Ustekinumab Trough Levels, Serum IL-22, and Oncostatin M Levels and Clinical and Biochemical Outcomes in Patients with Crohn's Disease.Journal of clinical medicine · 2024Article
72 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Polymorphisms of interleukin (IL)-23R and signaling components are associated with several autoimmune diseases, including inflammatory bowel diseases (IBD). Similar to T helper type 17 (Th17) lineage, type 3 innate lymphoid cells (ILCs) express retinoic acid-related orphan receptor γt (Rorγt) and IL-23R and hence, produce Th17-type cytokines. Recent reports implicated type 3 ILCs in IBD; however, how IL-23R signaling in these cells contributes to pathogenesis is unknown. IL-22, produced in copious amounts by type 3 ILCs, was reported to have both beneficial and pathogenic effects in adaptive, yet only a protective role in innate colitis models. Herein, by employing chronic CD45RB(high) CD4(+) T-cell transfer and anti-CD40 antibody-induced acute innate colitis models in Rag1(-/-) mice, we demonstrated opposite roles for IL-23R in colitogenesis: in the former a protective, and in the latter a pathogenic role. Furthermore, we show that IL-23R signaling promotes innate colitis via IL-22 as neutralization of IL-22 protected mice from colitis and adding back of IL-22 to IL-23R-deficient animals restored the disease. Collectively, our results reveal that similar to its controversial role during chronic or adaptive colitis, IL-22 may also have opposite roles in innate colitis pathogenesis in a context and insult-dependent manner.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.