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Inflammation

Th1/Th2 Cells

  • Chapter
Allergy and Allergic Diseases

  • 144 Accesses

Abstract

Atopic allergy is a genetically determined disorder characterized by an increased ability of B-lymphocytes to form immunoglobulin E (IgE) antibodies to certain groups of ubiquitous antigens that can activate the immune system after inhalation or ingestion, and perhaps after penetration through the skin (allergens). IgE antibodies are able to bind to high-affinity (type I) Fce receptors (FcεRI) present on the surface of mast cells/basophils, and allergen-induced FcεRI cross linking triggers the release of vasoactive mediators, chemotactic factors, and cytokines that are responsible for the allergic cascade. In addition to IgE-producing B-cells and IgE-binding mast cells/basophils, eosinophils also appear to be involved in the pathogenesis of allergic reactions, since these cells usually accumulate in the sites of allergic inflammation and the toxic products they release significantly contribute to the induction of tissue damage. The mechanisms accounting for the joint involvement of IgE-producing B-cells, mast cells/basophils, and eosinophils in the pathogenesis of allergic reactions had remained unclear until the existence of two polarized forms of the cluster differentiation (CD)4+ T-helper (Th) cell-mediated specific immune response, based on their profile of cytokine production and defined as type 1 T-helper (Thl) and type 2 T-helper (Th2), was discovered (1).

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Authors
  1. Sergio Romagnani MD
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Editors and Affiliations

  1. Department of Medicine, McMaster University, Hamilton, Ontario, Canada

    Judah A. Denburg MD, FRCP(C)

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© 1998 Springer Science+Business Media New York

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Romagnani, S. (1998). Inflammation. In: Denburg, J.A. (eds) Allergy and Allergic Diseases. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-4757-2776-0_11

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  • DOI: https://doi.org/10.1007/978-1-4757-2776-0_11

  • Publisher Name: Humana Press, Totowa, NJ

  • Print ISBN: 978-1-61737-026-7

  • Online ISBN: 978-1-4757-2776-0

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