ArticleThe Journal of investigative dermatology2012
IL-33: a novel danger signal system in atopic dermatitis.
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 54 papers.
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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.
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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
54 citing papers in PubMed, 112 citations in OpenAlex.
- Aeroallergens in Atopic Dermatitis and Chronic Urticaria.Current allergy and asthma reports · 2026Review
- Predicting Role of Interleukin-33 in Determining the Development and Severity of Atopic Dermatitis.Immunity, inflammation and disease · 2026Article
- Biological mechanisms and therapeutic prospects of interleukin-33 in pathogenesis and treatment of allergic disease.Journal of inflammation (London, England) · 2025Review
- IL-7 secreted by keratinocytes induces melanogenesis via c-kit/MAPK signaling pathway in Melan-a melanocytes.Archives of dermatological research · 2025Article
- Immunological Antagonism Between Psoriasis and Atopic Dermatitis: Pathways, Clinical Implications, and Therapeutic Perspectives.Clinical, cosmetic and investigational dermatology · 2025Review
- How underappreciated autoinflammatory (innate immunity) mechanisms dominate disparate autoimmune disorders.Frontiers in immunology · 2024Review
- Intrinsic Effects of Exposome in Atopic Dermatitis: Genomics, Epigenomics and Regulatory Layers.Journal of clinical medicine · 2023Review
- Promoting New Approach Methodologies (NAMs) for research on skin color changes in response to environmental stress factors: tobacco and air pollution.Frontiers in toxicology · 2023Review
- Phase 1 and 2 Randomized Clinical Studies Determine Lack of Efficacy for Anti-IL-17C Antibody MOR106 in Moderate-Severe Atopic Dermatitis.Journal of clinical medicine · 2022Article
- IL-33/Regulatory T-Cell Axis Suppresses Skin Fibrosis.The Journal of investigative dermatology · 2022Article
- Critical Players and Therapeutic Targets in Chronic Itch.International journal of molecular sciences · 2022Review
- Article
- Cell death in skin function, inflammation, and disease.The Biochemical journal · 2022Review
- Role of Damage-Associated Molecular Patterns (DAMPs/Alarmins) in Severe Ocular Allergic Diseases.Cells · 2022Review
- Molecular and cellular mechanisms of itch and pain in atopic dermatitis and implications for novel therapeutics.Clinical & translational immunology · 2022Review
- Atopic dermatitis: Is innate or adaptive immunity in control? A clinical perspective.Frontiers in immunology · 2022Review
- Deacetylasperulosidic Acid Ameliorates Pruritus, Immune Imbalance, and Skin Barrier Dysfunction in 2,4-Dinitrochlorobenzene-Induced Atopic Dermatitis NC/Nga Mice.International journal of molecular sciences · 2021Article
- Involvement of Alarmins in the Pathogenesis and Progression of Multiple Myeloma.International journal of molecular sciences · 2021Review
- Anti-Inflammatory and Anti-Allergic Effects of Saponarin and Its Impact on Signaling Pathways of RAW 264.7, RBL-2H3, and HaCaT Cells.International journal of molecular sciences · 2021Article
- Diversified Stimuli-Induced Inflammatory Pathways Cause Skin Pigmentation.International journal of molecular sciences · 2021Review
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2 authors at 1 institution in 1 country.
Funding
Abstract
IL-33 is a newly recognized cytokine of the IL-1 cytokine family that has recently been attributed to the epithelial "alarmin" defense system. IL-33 is released by the epithelial cells in various tissues and organs, including keratinocytes, endothelial cells, and immune cells. Recent reports have suggested that IL-33 might be a critical part of the innate immunity, although its precise role is as yet poorly understood. In several organs, IL-33 appears to drive T helper type 2 (Th2) responses, suggesting roles in allergic and atopic diseases, as well as in fibrosis. IL-33 exerts its effects by activating the ST2 (suppression of tumorigenicity 2)/IL-1 aR receptor on different types of cells, including mast cells and Th2 cells. The ST2 receptor is either expressed on the cell surface or shed from these cells (soluble ST2, sST2), thereby functioning as a "decoy" receptor. After binding to its receptor, IL-33 activates NF-κB, suggesting that it regulates the outcome of diseases such as atopic dermatitis. On the other hand, several studies have reported on the inhibitory effects of sST2 in inflammatory and fibrotic diseases, suggesting that IL-33/ST2 is a unique cytokine with potential pro- and anti-inflammatory effects.
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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.