ArticlePloS one2017
Continuous IL-23 stimulation drives ILC3 depletion in the upper GI tract and, in combination with TNFα, induces robust activation and a phenotypic switch of ILC3.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Skin-derived myeloid precursors and joint-resident fibroblasts spread psoriatic disease from skin to joints.Nature immunology · 2026Article
- Recipient tissue microenvironment determines developmental path of intestinal innate lymphoid progenitors.Nature communications · 2024Article
- A little ER stress isn't bad: the IRE1α/XBP1 pathway shapes ILC3 functions during intestinal inflammation.The Journal of clinical investigation · 2024Article
- Group 3 innate lymphoid cells in intestinal health and disease.Nature reviews. Gastroenterology & hepatology · 2024Review
- Article
- Article
- ILC3: a case of conflicted identity.Frontiers in immunology · 2023Review
- The impact of genetic background and sex on the phenotype of IL-23 induced murine spondyloarthritis.PloS one · 2021Article
- Barrier lymphocytes in spondyloarthritis.Current opinion in rheumatology · 2020Review
- Article
- The Pathogenesis of Ankylosing Spondylitis: an Update.Current rheumatology reports · 2019Review
- Activation of DR3 signaling causes loss of ILC3s and exacerbates intestinal inflammation.Nature communications · 2019Article
- Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the Interleukin (IL)-23/IL-23 receptor loci are associated with increased inflammatory bowel disease (IBD) susceptibility, and IL-23 neutralization has shown efficacy in early clinical trials. To better understand how an excess of IL-23 affects the gastrointestinal tract, we investigated chronic systemic IL-23 exposure in healthy wildtype mice. As expected, IL-23 exposure resulted in early activation of intestinal type 3 innate lymphoid cells (ILC3), followed by infiltration of activated RORγt+ T helper cells. Surprisingly, however, sustained IL-23 stimulus also dramatically reduced classical ILC3 populations within the proximal small intestine, and a phenotypically distinct T-bet expressing ILC3 population emerged. TNFα neutralization, a widely used IBD therapy, reduced several aspects of the IL-23 driven ILC3 response, suggesting a synergy between IL-23 and TNFα in ILC3 activation. In vitro studies supported these findings, revealing previously unappreciated effects of IL-23 and TNFα within the intestine.
Indexed as
Identifiers
What OpenQuestion holds
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.