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Eosinophils and Allergy in Asthma

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Eosinophils are recruited to the site of IgE-mediated allergic reaction in the airway in asthma. Major eosinophil-chemotactic factors released from mast cells are platelet activating factor and Leukotriene B4. In addition, T cells and bronchial epithelial cells produce eosinophil chemotactic cytokines. Cytokines including IL-5, IL-3, and GM-CSF, which are released mainly from CD4+ T cells and possibly Th2, activates eosinophils for migration, tissue damage, and survival. Adhesion molecules on eosinophils and constituent structures of the airway participate in the process of eosinophil migration. Among a variety of adhesion molecules, VLA-4 and VCAM-1 are unique to the interaction between eosinophils and endothelial cells. A major role of recruited eosinophils in the airway in asthma is considered to be damage to the bronchial epithelium caused by eosinophil specific granules proteins, in addition to production of lipid mediators, production of cytokines, antigen-presenting cell junction, and possible induction of basement membrane thickening in the airway.

Document Type: Research Article


Publication date: January 1, 1995

More about this publication?
  • Allergy and Asthma Proceedings is a peer reviewed publication dedicated to distributing timely scientific research regarding advancements in the knowledge and practice of allergy, asthma and immunology. Its primary readership consists of allergists and pulmonologists.

    The goal of the Proceedings is to publish articles with a predominantly clinical focus which directly impact quality of care for patients with allergic disease and asthma.

    Featured topics include asthma, rhinitis, sinusitis, food allergies, allergic skin diseases, diagnostic techniques, allergens, and treatment modalities. Published material includes peer-reviewed original research, clinical trials and review articles.

    Articles marked "F" offer free full text for personal noncommercial use only.

    The journal is indexed in Thomson Reuters Web of Science and Science Citation Index Expanded, plus the National Library of Medicine's PubMed service.
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