Hypersensitivity: Anaphylactic (Type I)

Gary A Bannon, Monsanto Company, St. Louis, Missouri, USA

Published online: January 2006

DOI: 10.1038/npg.els.0003999

Type I hypersensitivity reactions occur in individuals who have been previously sensitized to a specific allergen. They are the result of allergen recognition by immunoglobulin E on mast cells and basophils and cause a variety of symptoms such as itching or tingling of the lips, tongue or throat; nausea, vomiting and diarrhoea; sneezing, runny nose and wheezing, shortness of breath and coughing. In some cases, the reaction can be so severe that the circulatory system shuts down and tracheal swelling occurs, leading to a life-threatening condition known as anaphylaxis.

Keywords: IgE; allergens; B cells; mast cells; T cells

Figure 1. Interaction of the immune system with an allergen. On first exposure to an allergen, antigen-presenting cells (APCs) will take up, degrade, and then present allergen fragments (T-cell epitopes) to T cells. In a susceptible individual a TH2-type response will take place where the T cell will secrete cytokines and other mediators that cause the B cell to proliferate and produce immunoglobulin E (IgE). The IgE will be bound by mast cells through the IgE-binding receptor. On subsequent allergen exposures, the allergen will be bound by the mast cells causing a degranulation, or exocytosis, of its granular contents. The granular contents contain the chemicals and mediators (histamine) that cause the clinical symptoms of allergy.
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 Further Reading
    Golden DB (2003) Stinging insect allergy. American Family of Physician 15(12): 2541–2546.
    Herrick CA, Xu L, McKenzie AN, Tigelaar RE and Bottomly K (2003) IL-13 is necessary, not simply sufficient, for epicutaneously induced Th2 responses to soluble protein antigen. Journal of Immunology 170(5): 2488–2495.
    Huang SK (1998) Molecular modulation of allergic responses. Journal of Allergy and Clinical Immunology 102: 887–892.
    Kirman J and Le Gros G (1998) Which is the true regulator of TH2 cell development in allergic immune responses?. Clinical and Experimental Allergy 28: 908–910.
    Rolland J and O'Hehir R (1998) Immunotherapy of allergy: anergy, deletion, and immune deviation. Current Opinion in Immunology 10: 640–645.
    Spiegelberg HL, Takabayashi K, Beck L and Raz E (2002) DNA-based vaccines for allergic disease. Expert Reviews in Vaccines 1(2): 169–177.
    book Stanley JS and Bannon GA (2003) "Molecular mechanisms of food allergy". In: Zempleni J and Daniel H (eds) Molecular Nutrition, pp. 369–379. Wallingford, Oxon, UK: CABI Publishing.
    Sturm G, Kranke B, Rudolph C and Aberer W (2002) Rush Hymenoptera venom immunotherapy: a safe and practical protocol for high-risk patients. Journal of Allergy and Clinical Immunology 110(6): 928–933.

Related Sub-Topics:

Diagnostics, Therapeutics and Methods | Allergy and Hypersensitivity
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Article Title: Hypersensitivity: Anaphylactic (Type I)
 
How to Cite close
Bannon, Gary A(Jan 2006) Hypersensitivity: Anaphylactic (Type I). In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1038/npg.els.0003999]