| Literature DB >> 6699311 |
Abstract
In looking for an additional mechanism that could cause inflammation and therefore be important in the pathogenesis of asthma and rhinitis, IgG- and IgE-CIC were determined in a number of patients that were suffering from asthma and/or rhinitis. Patients were further subdivided into allergic (type I allergy) and nonallergic patients on the basis of history, skin testing with common inhalant allergens, RAST, and, if necessary, allergen provocation. In addition, a control group and patients that were undergoing allergen-specific hyposensitization were studied also. The mean level and frequency of elevated IgG-CIC were significantly increased in all three patient groups as compared to controls. The frequency of IgE-CIC was only significantly elevated in both allergic groups, and the difference between allergic and nonallergic patients was highly significant. IgG- and IgE-CIC did not increase during long-term allergen hyposensitization. Since there was no significant increase of IgE-CIC 10 min after bronchial allergen challenge nor at the moment that symptoms such as urticaria, bronchial obstruction, or rhinorrhea appeared during rush hyposensitization in asthmatic patients, we think that CIC are not involved in classic type I allergic reactions. The possible role of IgG- and IgE-CIC in inducing inflammatory, mediator release from eosinophils and macrophages via binding of Fc receptors on these cells is discussed.Entities:
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Year: 1984 PMID: 6699311 DOI: 10.1016/s0091-6749(84)80020-2
Source DB: PubMed Journal: J Allergy Clin Immunol ISSN: 0091-6749 Impact factor: 10.793