ArticleFrontiers in immunology2013
Opposing Functions of Classic and Novel IL-1 Family Members in Gut Health and Disease.
Article in Frontiers in immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.
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
77 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.
- Immunobiological Properties and Clinical Applications of Interleukin-38 for Immune-Mediated Disorders: A Systematic Review Study.International journal of molecular sciences · 2021Pooled it
- Differential Expression of IL-36 Family Members and IL-38 by Immune and Nonimmune Cells in Patients with Active Inflammatory Bowel Disease.BioMed research international · 2018Trial
- Ulcerative colitis: from molecular pathophysiology to management and the emerging role of natural and pharmacological drug candidates.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Unraveling the Converging Roles of ASC-Dependent Inflammasomes, Interleukin-1 Superfamily Members, Serum Amyloid A, and Non-Sterile Inflammation in Disease Pathology and Fibrosis in Inflammatory Bowel Disease and Primary Sclerosing Cholangitis.International journal of molecular sciences · 2025Review
- Reduction of colitis in mice by chemically programmed supramolecular nanoassemblies of vitamin-lipid conjugates.Journal of nanobiotechnology · 2025Article
- Tumor-infiltrating mast cells stimulate ICOSJournal of advanced research · 2024Article
- Study on the effect and mechanism ofFrontiers in microbiology · 2024Article
- The role and mechanism of TXNDC5 in disease progression.Frontiers in immunology · 2024Review
- Gut instinct: harnessing the power of probiotics to tame pathogenic signaling pathways in ulcerative colitis.Frontiers in medicine · 2024Review
- miR-369-3p Modulates Intestinal Inflammatory Response via BRCC3/NLRP3 Inflammasome Axis.Cells · 2023Article
- Expression of IL-21 and IL-33 in Intestinal Mucosa of Inflammatory Bowel Disease: An Immunohistochemical Study.Diagnostics (Basel, Switzerland) · 2023Article
- NOD1 mediates interleukin-18 processing in epithelial cells responding to Helicobacter pylori infection in mice.Nature communications · 2023Article
- Effects ofAnimals : an open access journal from MDPI · 2023Article
- Dual function of fungi-derived cytokines in inflammatory bowel diseases: protection or inflammation.Gastroenterology report · 2023Review
- Review
- IL-33 and IL-37: A Possible Axis in Skin and Allergic Diseases.International journal of molecular sciences · 2022Review
- Cytokine Mixtures Mimicking the Local Milieu in Patients with Inflammatory Bowel Disease Impact Phenotype and Function of Mesenchymal Stromal Cells.Stem cells translational medicine · 2022Article
- Involvement of IL-33 in the Pathophysiology of Systemic Lupus Erythematosus: Review.International journal of molecular sciences · 2022Review
- Interleukin-37 exacerbates experimental colitis in an intestinal microbiome-dependent fashion.Theranostics · 2022Article
- Role of Pyroptosis in Inflammatory Bowel Disease (IBD): From Gasdermins to DAMPs.Frontiers in pharmacology · 2022Review
17 more citing papers are in PubMed but not listed here.
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 at 1 institution in 2 countries.
Funding
Abstract
In addition to their well-established role(s) in the pathogenesis of gastrointestinal (GI)-related inflammatory disorders, including inflammatory bowel disease (IBD) and inflammation-associated colorectal cancer (CRC), emerging evidence confirms the critical involvement of the interleukin-1 (IL-1) cytokine family and their ligands in the maintenance of normal gut homeostasis. In fact, the paradigm that IBD occurs in two distinct phases is substantiated by the observation that classic IL-1 family members, such as IL-1, the IL-1 receptor antagonist (IL-1Ra), and IL-18, possess dichotomous functions depending on the phase of disease, as well as on their role in initiating vs. sustaining chronic gut inflammation. Another recently characterized IL-1 family member, IL-33, also possesses dual functions in the gut. IL-33 is upregulated in IBD and potently induces Th2 immune responses, while also amplifying Th1-mediated inflammation. Neutralization studies in acute colitis models, however, have yielded controversial results and recent reports suggest a protective role of IL-33 in epithelial regeneration and mucosal wound healing. Finally, although little is currently known regarding the potential contribution of IL-36 family members in GI inflammation/homeostasis, another IL-1 family member, IL-37, is emerging as a potent anti-inflammatory cytokine with the ability to down-regulate colitis. This new body of information has important translational implications for both the prevention and treatment of patients suffering from IBD and inflammation-associated CRC.
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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.