ArticleMucosal immunology2017
Intelectin contributes to allergen-induced IL-25, IL-33, and TSLP expression and type 2 response in asthma and atopic dermatitis.
Article in Mucosal immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.
- IL-33/IL-31 Axis in Immune-Mediated and Allergic Diseases.International journal of molecular sciences · 2019Pooled it
- Intelectin-2 is a broad-spectrum antimicrobial lectin.Nature communications · 2026Article
- Susceptibility of mice to primaryFrontiers in immunology · 2026Article
- Exploring the role of intelectin-1 in modulating asthma through the gut-bone-lung axis.Gut microbes · 2025Article
- IL-31/33 Axis in Atopic Dermatitis.International journal of molecular sciences · 2025Review
- The immunology of asthma.Nature immunology · 2025Review
- Omentin-General Overview of Its Role in Obesity, Metabolic Syndrome and Other Diseases; Problem of Current Research State.Biomedicines · 2025Review
- ITLN1 exacerbates Crohn's colitis by driving ZBP1-dependent PANoptosis in intestinal epithelial cells through antagonizing TRIM8-mediated CAPN2 ubiquitination.International journal of biological sciences · 2025Article
- Mast cell-neuron axis as a core mechanism in chronic pruritus of atopic dermatitis: from mechanistic insights to therapeutic targets.Frontiers in immunology · 2025Review
- Soluble Human Lectins at the Host-Microbe Interface.Annual review of biochemistry · 2024Review
- Exploring the Role of Lactoferrin in Managing Allergic Airway Diseases among Children: Unrevealing a Potential Breakthrough.Nutrients · 2024Review
- The Role of Peptides in Asthma-Obesity Phenotype.International journal of molecular sciences · 2024Review
- Adipokine levels and their association with clinical disease severity in patients with dengue.PLoS neglected tropical diseases · 2023Article
- Disease modification in inflammatory skin disorders: opportunities and challenges.Nature reviews. Drug discovery · 2023Review
- Diagnostic and Prognostic Value of Serum Omentin-1 in Sepsis: A Prospective Study in Critically Ill Patients.Medicina (Kaunas, Lithuania) · 2023Article
- Severe Asthmatic Responses: The Impact of TSLP.International journal of molecular sciences · 2023Review
- Adipokine levels and their association with clinical disease severity in patients with dengue.medRxiv : the preprint server for health sciences · 2023Article
- The role of the novel adipokines vaspin and omentin in chronic inflammatory diseases.Pediatric endocrinology, diabetes, and metabolism · 2023Review
- Knowledge mapping and research trends of IL-33 from 2004 to 2022: a bibliometric analysis.Frontiers in immunology · 2023Article
- Biologics and airway remodeling in severe asthma.Allergy · 2022Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
The epithelial and epidermal innate cytokines IL-25, IL-33, and thymic stromal lymphopoietin (TSLP) have pivotal roles in the initiation of allergic inflammation in asthma and atopic dermatitis (AD). However, the mechanism by which the expression of these innate cytokines is regulated remains unclear. Intelectin (ITLN) is expressed in airway epithelial cells and promotes allergic airway inflammation. We hypothesized that ITLN is required for allergen-induced IL-25, IL-33, and TSLP expression. In two asthma models, Itln knockdown reduced allergen-induced increases in Il-25, Il-33, and Tslp and development of type 2 response, eosinophilic inflammation, mucus overproduction, and airway hyperresponsiveness. Itln knockdown also inhibited house dust mite (HDM)-induced early upregulation of Il-25, Il-33, and Tslp in a model solely inducing airway sensitization. Using human airway epithelial cells, we demonstrated that HDM-induced increases in ITLN led to phosphorylation of epidermal growth factor receptor and extracellular-signal regulated kinase, which were required for induction of IL-25, IL-33, and TSLP expression. In two AD models, Itln knockdown suppressed expression of Il-33, Tslp, and Th2 cytokines and eosinophilic inflammation. In humans, ITLN1 expression was significantly increased in asthmatic airways and in lesional skin of AD. We conclude that ITLN contributes to allergen-induced Il-25, Il-33, and Tslp expression in asthma and AD.
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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.