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Anti-Inflammatory Drugs in Asthma pp 215–227Cite as

Birkhäuser

Anti-IgE Agents

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Part of the book series: Progress in Inflammation Research ((PIR))

Abstract

There is little debate over the essential role of IgE in allergic reactions. During an allergic response, CD4+ T lymphocytes of the Th2 phenotype stimulate allergen-specific B cells to produce IgE molecules via the release of IL-4/IL-13. The receptors for IgE are found on a multitude of different cells and two different types have been identified: the high-affinity receptor (FcεRI) on mast cells, basophils, and antigen-presenting cells, and the low-affinity receptor (FcεRII or CD23) on B lymphocytes, monocytes/macrophages, eosinophils, dendritic cells, and epithelial cells. After interaction with allergens, IgE-armed cells release a number of inflammatory mediators and enhance and redirect antigen presentation. This cascade of events seems to have a crucial role in the generation and persistence of symptoms in allergic diseases. The development of drugs that interfere with IgE production and function may therefore represent a more specific approach to treat these pathological conditions [1, 2].

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Authors and Affiliations

  1. Project Management, Novartis Pharma A.G., S-386.12.15, CH-4002, Basel, Switzerland

    Francesco Patalano

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  1. Francesco Patalano
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  1. Immunopharmacology Group, Southampton General Hospital, Tremona Road, Southampton, SO16 6YD, UK

    Anthony P. Sampson  & Martin K. Church  & 

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Patalano, F. (1999). Anti-IgE Agents. In: Sampson, A.P., Church, M.K. (eds) Anti-Inflammatory Drugs in Asthma. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8751-9_8

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  • DOI: https://doi.org/10.1007/978-3-0348-8751-9_8

  • Publisher Name: Birkhäuser, Basel

  • Print ISBN: 978-3-0348-9757-0

  • Online ISBN: 978-3-0348-8751-9

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