ReviewFrontiers in immunology2018
Regulatory Mechanisms of IL-33-ST2-Mediated Allergic Inflammation.
Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 88 citations in OpenAlex.
- The Elevated Soluble ST2 Predicts No-Reflow Phenomenon in ST-Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention.Journal of atherosclerosis and thrombosis · 2019Trial
- Rewiring Atopic Dermatitis: Alarmin Cytokines at the Core of Barrier-Immune-Neuro-Microbiome Networks.Clinical reviews in allergy & immunology · 2026Review
- Constitutively high levels of endogenous soluble ST2 inhibit food allergic responses in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- IL-33 induces stronger responses in female mast cells and neutrophils: a role for the JNK pathway.Frontiers in immunology · 2026Article
- Impact of Transport Media on IL-33 Levels in Samples From Patients With Viral Respiratory Infections.Journal of immunology research · 2026Article
- Baicalin restores innate lymphoid immune imbalance during exacerbation of COPD.Immunologic research · 2025Article
- Article
- Stem cells, Notch-1 signaling, and oxidative stress: a hellish trio in cancer development and progression within the airways. Is there a role for natural compounds?Carcinogenesis · 2024Review
- Article
- Associations ofHeliyon · 2024Article
- Interleukin 33 supports squamous cell carcinoma growth via a dual effect on tumour proliferation, migration and invasion, and T cell activation.Cancer immunology, immunotherapy : CII · 2024Article
- Article
- A Novel Bionebulizer Approach to Study the Effects of Natural Mineral Water on a 3D In Vitro Nasal Model from Allergic Rhinitis Patients.Biomedicines · 2024Article
- A tuft cell - ILC2 signaling circuit provides therapeutic targets to inhibit gastric metaplasia and tumor development.Nature communications · 2023Article
- RORα overexpression reduced interleukin-33 expression and prevented mast cell degranulation and inflammation by inducing autophagy in allergic rhinitis.Immunity, inflammation and disease · 2023Article
- Knowledge mapping of interleukin-33: a bibliometric study.American journal of translational research · 2023Article
- Advances in understanding of the pathogenesis and therapeutic implications of drug reaction with eosinophilia and systemic symptoms: an updated review.Frontiers in medicine · 2023Review
- Increased expression of IL1-RL1 is associated with type 2 and type 1 immune pathways in asthma.BMC immunology · 2022Article
- The role of interleukin-33 in organ fibrosis.Discovery immunology · 2022Review
- Predictive Values of Serum IL-33 and sST2 in Endotypes and Postoperative Recurrence of Chronic Rhinosinusitis with Nasal Polyps.Mediators of inflammation · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-33 (IL-33) plays multiple roles in tissue homeostasis, prevention of parasitic infection, and induction of allergic inflammation. Especially, IL-33-ST2 (IL-1RL1) axis has been regarded as the villain in allergic diseases such as asthma and atopic dermatitis and in autoimmune diseases such as rheumatoid arthritis. Indeed, a number of studies have indicated that IL-33 produced by endothelial cells and epithelial cells plays a critical role in the activation and expansion of group 2 innate lymphoid cells (ILC2s) which cause allergic inflammation by producing large amounts of IL-5 and IL-13. However, mechanisms that antagonize IL-33-ST2-mediated allergic responses remain largely unknown. Recently, several groups including our group have demonstrated cellular and molecular mechanisms that could suppress excessive activation of ILC2s by the IL-33-ST2 axis. In this review, we summarize recent progress in the regulatory mechanisms of IL-33-ST2-mediated allergic responses. Selective targeting of the IL-33-ST2 axis would be a promising strategy in the treatment of allergic diseases.
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.