Abstract
Allergic inflammation, caused by development of an allergen-induced immune response, is largely driven via immunoglobulin E (IgE)-dependent mechanisms. It manifests clinically as asthma, rhinoconjunctivitis (more commonly known as hay fever), allergic skin inflammation (the main example of which is atopic dermatitis), food allergy, urticaria, and/or anaphylaxis, with several known disease variants caused by different underlying cellular and molecular mechanisms (1). Increased levels of circulating IgE, allergen-specific IgE reactivity profiles measured with radioallergosorbent tests and positive skin prick tests for specific allergens, together with auxiliary ex vivo and in vitro mast cell and basophil activation functional readouts, support the importance of IgE antibodies in the clinical manifestation of allergies (2, 3). Allergic inflammation can be local (that is, within the target organ), as is the case for allergic rhinoconjunctivitis and allergic asthma, or systemic, as is the case for anaphylaxis. The etiology of allergic immune responses has been shown to be influenced by several factors, including genetic susceptibility (4), route of exposure, dose of the allergen, and in some cases, structural characteristics of the allergen (5).
Original language | English |
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Title of host publication | Antibodies for Infectious Diseases |
Publisher | WILEY-BLACKWELL |
Pages | 75-102 |
Number of pages | 28 |
ISBN (Electronic) | 9781683670988 |
ISBN (Print) | 9781555817350 |
DOIs | |
Publication status | Published - 26 May 2015 |
Keywords
- Allergic diseases
- Cancer therapy
- Corticosteroid treatment
- Immune inflammation
- Immunoglobulin E antibodies
- Immunological mechanisms
- Infectious diseases