ArticleInternational immunology2009
Ablation of type I hypersensitivity in experimental allergic conjunctivitis by eotaxin-1/CCR3 blockade.
Article in International immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 35 citations in OpenAlex.
- The role of mast cells in allergic rhinitis.PeerJ · 2025Review
- Allergic Conjunctivitis: Review of Current Types, Treatments, and Trends.Life (Basel, Switzerland) · 2024Review
- Compilation of Evidence Supporting the Role of a T Helper 2 Reaction in the Pathogenesis of Acute Appendicitis.International journal of molecular sciences · 2024Review
- Ocular redness - II: Progress in development of therapeutics for the management of conjunctival hyperemia.The ocular surface · 2021Review
- CCR3-shRNA promotes apoptosis and inhibits chemotaxis and degranulation of mouse mast cells.Experimental and therapeutic medicine · 2020Article
- Role of the ocular surface microbiome in allergic disease.Current opinion in allergy and clinical immunology · 2019Review
- CCR3 Monoclonal Antibody Inhibits Eosinophilic Inflammation and Mucosal Injury in a Mouse Model of Eosinophilic Gastroenteritis.Allergy, asthma & immunology research · 2017Article
- Role of CCL7 in Type I Hypersensitivity Reactions in Murine Experimental Allergic Conjunctivitis.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Total IgE and eotaxin (CCL11) contents in tears of patients suffering from seasonal allergic conjunctivitis.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2014Article
- Comparison of effects of alcaftadine and olopatadine on conjunctival epithelium and eosinophil recruitment in a murine model of allergic conjunctivitis.Drug design, development and therapy · 2011Article
- Development of a T(H)17 immune response during the induction of murine syngeneic graft-versus-host disease.Cytokine · 2010Article
- Article
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
Abstract
The immune response is regulated, in part, by effector cells whose activation requires multiple signals. For example, T cells require signals emanating from the T cell antigen receptor and co-stimulatory molecules for full activation. Here, we present evidence indicating that IgE-mediated hypersensitivity reactions in vivo also require cognate signals to activate mast cells. Immediate hypersensitivity reactions in the conjunctiva are ablated in mice deficient in eotaxin-1, despite normal numbers of tissue mast cells and levels of IgE. To further define the co-stimulatory signals mediated by chemokine receptor 3 (CCR3), an eotaxin-1 receptor, effects of CCR3 blockade were tested with an allergic conjunctivitis model and in ex vivo isolated connective tissue-type mast cells. Our results show that CCR3 blockade significantly suppresses allergen-mediated hypersensitivity reactions as well as IgE-mediated mast cell degranulation. We propose that a co-stimulatory axis by CCR3, mainly stimulated by eotaxin-1, is pivotal in mast cell-mediated hypersensitivity reactions.
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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.