ReviewInflammatory bowel diseases2014
Interleukin 23 in Crohn's disease.
Review in Inflammatory bowel diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
19 citing papers in PubMed.
- Phantom of the immunologic opera: Unmasking the role of innate lymphoid cells (ILC) in inborn errors of immunity (IEI).Journal of human immunity · 2025Review
- Main genetic factors associated with inflammatory bowel diseases and their consequences on intestinal permeability: involvement in gut inflammation.Journal of gastroenterology · 2025Review
- Effects of CB2 Receptor Modulation on Macrophage Polarization in Pediatric Inflammatory Bowel Disease.International journal of molecular sciences · 2025Article
- Pharmacological Inhibition of N-Acylethanolamine Acid Amidase (NAAA) Mitigates Intestinal Fibrosis Through Modulation of Macrophage Activity.Journal of Crohn's & colitis · 2025Article
- Importance of Fecal Microbiota Transplantation and Molecular Regulation as Therapeutic Strategies in Inflammatory Bowel Diseases.Nutrients · 2024Review
- Risankizumab: Mechanism of action, clinical and translational science.Clinical and translational science · 2024Review
- Spondyloarthritis with inflammatory bowel disease: the latest on biologic and targeted therapies.Nature reviews. Rheumatology · 2023Review
- Alterations of the Skin and Gut Microbiome in Psoriasis and Psoriatic Arthritis.International journal of molecular sciences · 2021Review
- Genetic and Environmental Determinants of T Helper 17 Pathogenicity in Spondyloarthropathies.Frontiers in genetics · 2021Review
- Role of the IL23/IL17 Pathway in Crohn's Disease.Frontiers in immunology · 2021Review
- Relationship between theInternational journal of environmental research and public health · 2019Article
- Psoriasis Pathogenesis and Treatment.International journal of molecular sciences · 2019Review
- IL-15 negatively regulates curdlan-induced IL-23 production by human monocyte-derived dendritic cells and subsequent Th17 response.Northern clinics of Istanbul · 2019Article
- Human Gut-Associated Natural Killer Cells in Health and Disease.Frontiers in immunology · 2019Review
- Peyer's patch myeloid cells infection byThe Journal of experimental medicine · 2018Article
- Article
- Stromal C-type lectin receptor COLEC12 integrates H. pylori, PGE2-EP2/4 axis and innate immunity in gastric diseases.Scientific reports · 2018Article
- NK cells are biologic and biochemical targets of 6-mercaptopurine in Crohn's disease patients.Clinical immunology (Orlando, Fla.) · 2017Article
- Elevated IL-23R Expression and Foxp3+Rorgt+ Cells in Intestinal Mucosa During Acute and Chronic Colitis.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
: Crohn's disease (CD) is a lifelong inflammatory condition with underlying environmental and genetic components. CD affects multiple parts of the gastrointestinal tract, and it has a growing incidence in Western societies. IL-23 receptor variants have been identified as susceptibility or resistance factors for CD in genome-wide association studies. Accordingly, IL-23 is required for the development of experimental inflammatory bowel disease in many murine models. IL-23 receptor is expressed by both innate and adaptive immune cells, which include Th17, natural killer T, γδ T cells, and RORγt innate lymphoid cells all of which are capable of secreting IL-17A, IL-17F, IL-22, and interferon-γ upon IL-23 stimulation. During the past decade, pathogenic and protective roles have been described for these cytokines in the inflammatory bowel disease pathogenesis. More recently, innate lymphoid cells have been implicated in disease development. In this review, we have summarized and discussed these findings with an emphasis not only on the contribution of Th17 but also on innate lymphoid cells to disease etiology.
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.