ArticleAllergy2011
A potential new target for asthma therapy: a disintegrin and metalloprotease 10 (ADAM10) involvement in murine experimental asthma.
Article in Allergy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 49 citations in OpenAlex.
- A Valuable Target for Therapy: The Metalloproteinase ADAM10.Current protein & peptide science · 2025Review
- Regulation of ADAM10 by the TspanC8 Family of Tetraspanins and Their Therapeutic Potential.International journal of molecular sciences · 2021Review
- miR-23b Negatively Regulates Sepsis-Induced Inflammatory Responses by Targeting ADAM10 in Human THP-1 Monocytes.Mediators of inflammation · 2019Article
- Allergen Delivery Inhibitors: A Rationale for Targeting Sentinel Innate Immune Signaling of Group 1 House Dust Mite Allergens through Structure-Based Protease Inhibitor Design.Molecular pharmacology · 2018Review
- Proteolytic ectodomain shedding of membrane proteins in mammals-hardware, concepts, and recent developments.The EMBO journal · 2018Review
- ADAM10 and Notch1 on murine dendritic cells control the development of type 2 immunity and IgE production.Allergy · 2018Article
- Renal ADAM10 and 17: Their Physiological and Medical Meanings.Frontiers in cell and developmental biology · 2018Article
- Regulation of Leukocytes by TspanC8 Tetraspanins and the "Molecular Scissor" ADAM10.Frontiers in immunology · 2018Review
- ADAM10-Mediated ICOS Ligand Shedding on B Cells Is Necessary for Proper T Cell ICOS Regulation and T Follicular Helper Responses.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Scissor sisters: regulation of ADAM10 by the TspanC8 tetraspanins.Biochemical Society transactions · 2017Review
- Allergen-dependent oxidant formation requires purinoceptor activation of ADAM 10 and prothrombin.The Journal of allergy and clinical immunology · 2017Article
- Fine Tuning Cell Migration by a Disintegrin and Metalloproteinases.Mediators of inflammation · 2017Review
- A time-varying group sparse additive model for genome-wide association studies of dynamic complex traits.Bioinformatics (Oxford, England) · 2016Article
- Article
- Inhibition of CD23-mediated IgE transcytosis suppresses the initiation and development of allergic airway inflammation.Mucosal immunology · 2015Article
- An ADAM10 promoter polymorphism is a functional variant in severe sepsis patients and confers susceptibility to the development of sepsis.Critical care (London, England) · 2015Article
- Abrogation of airway hyperresponsiveness but not inflammation by rho kinase insufficiency.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2015Article
- Article
- ADAM10 is required for SCF-induced mast cell migration.Cellular immunology · 2014Article
- A specific sphingosine kinase 1 inhibitor attenuates airway hyperresponsiveness and inflammation in a mast cell-dependent murine model of allergic asthma.The Journal of allergy and clinical immunology · 2013Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundElevated levels of CD23, a natural regulator of IgE production, have been shown to decrease the signs of lung inflammation in mice. The aim of this study was to study the involvement of ADAM10, the primary CD23 sheddase, in experimental asthma.
methodsADAM10 was blocked either by using mice with a B-cell-specific deletion of the protease or pharmacologically by intranasal administration of selective ADAM10 inhibitors. Airway hypersensitivity (AHR) and bronchoaveolar lavage fluid (BALF) eosinophilia and select BALF cytokine/chemokine levels were then determined.
resultsUsing an IgE and mast cell-dependent mouse model, B-cell-specific ADAM10(-/-) mice (C57B/6 background) exhibited decreased eosinophilia and AHR when compared with littermate (LM) controls. Treatment of C57B/6 mice with selective inhibitors of ADAM10 resulted in an even further decrease in BALF eosinophilia, as compared with the ADAM10(-/-) animals. Even in the Th2 selective strain, Balb/c, BALF eosinophilia was reduced from 60% to 23% respectively. In contrast, when an IgE/mast cell-independent model of lung inflammation was used, the B-cell ADAM10(-/-) animals and ADAM10 inhibitor treated animals had lung inflammation levels that were similar to the controls.
conclusionsThese results thus show that ADAM10 is important in the progression of IgE-dependent lung inflammation. The use of the inhibitor further suggested that ADAM10 was important for maintaining Th2 levels in the lung. These results thus suggest that decreasing ADAM10 activity could be beneficial in controlling asthma and possibly other IgE-dependent diseases.
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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.