ArticleThe Journal of investigative dermatology2012
IL-33 and ST2 in atopic dermatitis: expression profiles and modulation by triggering factors.
Article in The Journal of investigative dermatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 171 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
171 citing papers in PubMed, 2 syntheses or guidelines pooled it, 376 citations in OpenAlex.
- Keratinocytes as active regulators of cutaneous and mucosal immunity: a systematic review across inflammatory epithelial disorders.Frontiers in immunology · 2025Pooled it
- IL-33/IL-31 Axis in Immune-Mediated and Allergic Diseases.International journal of molecular sciences · 2019Pooled it
- Pharmacokinetics and pharmacodynamics of itepekimab in adults with moderate-to-severe atopic dermatitis: Results from two terminated phase II trials.Clinical and translational science · 2024Trial
- A Novel Multi-Component Formulation Reduces Inflammation In Vitro and Clinically Lessens the Symptoms of Chronic Eczematous Skin.International journal of molecular sciences · 2023Trial
- Tacrolimus improved the pregnancy outcomes of patients with refractory recurrent spontaneous abortion and immune bias disorders: a randomized controlled trial.European journal of clinical pharmacology · 2023Trial
- The first-in-human study of CNTO 7160, an anti-interleukin-33 receptor monoclonal antibody, in healthy subjects and patients with asthma or atopic dermatitis.British journal of clinical pharmacology · 2020Trial
- IL-33 as a boundary-tissue state-transfer signal: a Reader-Alarmin-Effector architecture linking CNS and skin.Brain, behavior, & immunity - health · 2026Review
- Extracellular vesicles derived from the lactic acid bacterium Enterococcus rotai suppress melanogenesis by modulating the cAMP-MITF pathway.Bioresources and bioprocessing · 2026Article
- Mechanism of Gu-Ben-Hua-Shi (AESS) Formula Regulating Autophagy Through Hippo-YAP Pathway in Restoring the Skin Barrier in Atopic Dermatitis.Journal of cellular and molecular medicine · 2026Observational
- Rewiring Atopic Dermatitis: Alarmin Cytokines at the Core of Barrier-Immune-Neuro-Microbiome Networks.Clinical reviews in allergy & immunology · 2026Review
- Article
- Cytokines Associated with Activation of CD4International journal of molecular sciences · 2026Review
- Predicting Role of Interleukin-33 in Determining the Development and Severity of Atopic Dermatitis.Immunity, inflammation and disease · 2026Article
- Targeted therapies in atopic dermatitis: toward endotype-driven precision medicine and disease modification.Frontiers in immunology · 2026Review
- Therapeutic effect of an MRGPRX2/MRGPRB2 antagonist on LL-37-induced rosacea-like inflammation in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- S. aureus exposure during cutaneous antigen sensitization causes basophil- and interleukin-4-dependent exaggerated food anaphylaxis.Immunity · 2025Article
- Serum Soluble ST2 and IL-33 Levels in Finnish Patients With Juvenile Idiopathic Arthritis.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2025Article
- IL-31/33 Axis in Atopic Dermatitis.International journal of molecular sciences · 2025Review
- The anionic surfactant Sodium Dodecyl Benzene Sulfonate alleviates inflammatory responses in atopic dermatitis via NFκB/MAPK pathways in a STAT3-dependent manner.Scientific reports · 2025Article
- The IL-33/ST2 axis and tissue Treg maintain epithelial homeostasis and restrain cancer development in the skin.Cell reports · 2025Article
111 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the acute phase of atopic dermatitis (AD), T-helper type 2 (Th2) cytokines characterize the inflammatory response in the skin. IL-33 is a new tissue-derived cytokine, which is mainly expressed by cells of barrier tissues, and is known to activate Th2 lymphocytes, mast cells, and eosinophils. IL-33 signals through a receptor complex consisting of IL-33-specific receptor ST2 and a co-receptor IL-1RAcP. As IL-33 is known to promote Th2-type immunity, we examined expression profiles of IL-33 and its receptor components in human AD skin, in the murine model of AD, and in various cell models. We found increased expression of IL-33 and ST2 in AD skin after allergen or staphylococcal enterotoxin B (SEB) exposure, as well as in the skin of 22-week-old filaggrin-deficient mice. In addition, skin fibroblasts, HaCaT keratinocytes, primary macrophages, and HUVEC endothelial cells efficiently produced IL-33 in response to the combined stimulation of tumor necrosis factor-α and IFN-γ, which was further enhanced by a mimetic of double-stranded RNA. Finally, the increased expression of IL-33 and ST2 caused by irritant, allergen, or SEB challenge was suppressed by topical tacrolimus treatment. These results suggest an important role for IL-33-ST2 interaction in AD and highlight the fact that bacterial and viral infections may increase the production of IL-33.
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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.