ArticleMucosal immunology2018
IL-33 promotes gastrointestinal allergy in a TSLP-independent manner.
Article in Mucosal immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 43 papers, 1 of them a synthesis that pooled it.
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
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- IL-33/IL-31 Axis in Immune-Mediated and Allergic Diseases.International journal of molecular sciences · 2019Pooled it
- Multidimensional study of the oral microbiome, metabolite, and immunologic environment in peanut allergy.The Journal of allergy and clinical immunology · 2021Trial
- Trial
- S. aureus exposure during cutaneous antigen sensitization causes basophil- and interleukin-4-dependent exaggerated food anaphylaxis.Immunity · 2025Article
- Biological mechanisms and therapeutic prospects of interleukin-33 in pathogenesis and treatment of allergic disease.Journal of inflammation (London, England) · 2025Review
- Skin damage signals mediate allergic sensitization to spatially unlinked antigen.Science immunology · 2025Article
- Myeloid-derived IL-33 drives γδ T cell-dependent resistance against cutaneous infection by Strongyloides ratti.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Epithelial-immune interactions govern type 2 immunity at barrier surfaces.Current opinion in immunology · 2024Review
- Article
- MrgprA3 neurons drive cutaneous immunity against helminths through selective control of myeloid-derived IL-33.Nature immunology · 2024Article
- Atopic dermatitis and food allergy: More than sensitization.Mucosal immunology · 2024Review
- Pathogenic mechanisms in the evolution of food allergy.Immunological reviews · 2024Review
- Dietary fiber is a critical determinant of pathologic ILC2 responses and intestinal inflammation.The Journal of experimental medicine · 2024Article
- Skin biomarkers predict the development of food allergy in early life.The Journal of allergy and clinical immunology · 2024Article
- From the bench to the clinic: basophils and type 2 epithelial cytokines of thymic stromal lymphopoietin and IL-33.Clinical & translational immunology · 2024Review
- Targeting type 2 immunity and the future of food allergy treatment.The Journal of experimental medicine · 2023Review
- Beyond allergic progression: From molecules to microbes as barrier modulators in the gut-lung axis functionality.Frontiers in allergy · 2023Review
- Preclinical evaluation of alternatives to oral immunotherapy for food allergies.Frontiers in allergy · 2023Review
- Immune Responses at Host Barriers and Their Importance in Systemic Autoimmune Diseases.Advances in experimental medicine and biology · 2023Review
- Pericytes modulate islet immune cells and insulin secretion through Interleukin-33 production in mice.Frontiers in endocrinology · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Atopic dermatitis (AD) often precedes asthma and food allergy, indicating that epicutaneous sensitization to allergens may be important in the induction of allergic responses at other barrier surfaces. Thymic stromal lymphopoietin (TSLP) and interleukin (IL)-33 are two cytokines that may drive type 2 responses in the skin; both are potential targets in the treatment of allergic diseases. We tested the functional role of IL-33 and the interplay between IL-33 and TSLP in mouse models of atopic march and gastrointestinal (GI) allergy. IL-33-driven allergic disease occurred in a TSLP-independent manner. In contrast, mice lacking IL-33 signaling were protected from onset of allergic diarrhea in TSLP-driven disease. Epithelial-derived IL-33 was important in this model, as specific loss of IL-33 expression in the epithelium attenuated cutaneous inflammation. Notably, the development of diarrhea following sensitization with TLSP plus antigen was ameliorated even when IL-33 was blocked after sensitization. Thus, IL-33 has an important role during early cutaneous inflammation and during challenge. These data reveal critical roles for IL-33 in the "atopic march" that leads from AD to GI allergy.
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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.