New trends on the pathogenetic aspects of allergic bronchial asthma.
The central role of IgE antibodies in allergic bronchial asthma (ABA) is not disputed any longer. Immunological mechanisms other than IgE-mediated reactions in the pathogenesis of ABA have not yet been definitely demonstrated. There is controversy as to whether IgG STS antibodies, probably IgG4, play a role in the disease process. There is no evidence to support the involvement of immune complexes. Anti-beta-2-adrenergic receptor autoimmune responses cannot be considered as responsible for the development of the disease at the present time. In the last few years a great effort has been made to understand the immunological mechanisms underlying the enhanced and long-standing IgE antibody production in atopic diseases. The results obtained in different laboratories, including our own, are in favor of a high responder status to allergen epitopes in a large proportion of atopics and suggest that a preferential expression of IgE isotype in the antibody responses may occur through different mechanisms. Of great interest is the recent demonstration of IgE-binding factors with IgE-potentiating and suppressive activity and of other related regulatory molecules and receptors. Progress has been recently achieved in the characterization of mediators responsible for the different pathological changes of ABA. A linkage between immediate IgE-mediated reactions, bronchial late-phase reactions (LPR) and chronic inflammation (CI) has been reported. It has been demonstrated that a cascade of mediators and cell interactions induce both LPR and CI. There is evidence of a close relationship between LPR-CI and nonspecific bronchial hyperreactivity. A better knowledge of pathogenetic mechanisms of ABA would open new perspectives in the therapy. A modulation of IgE antibody production can be attempted in different ways. At present a control of mediator release and of airway hyperreactivity can be achieved by several pharmacological interventions and by the avoidance of common and/or occupational allergens or pollutants.
D000485:Allergens / Q000276:immunology; D000486:Allergy and Immunology / Q000639:trends*; D000917:Antibody Formation; D001249:Asthma / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D001402:B-Lymphocytes / Q000502:physiology; D001696:Biomechanical Phenomena; D006801:Humans; D006967:Hypersensitivity / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D006969:Hypersensitivity, Immediate / Q000235:genetics / Q000276:immunology / Q000503:physiopathology; D007073:Immunoglobulin E / Q000096:biosynthesis / Q000276:immunology / Q000378:metabolism; D007132:Immunoglobulin Isotypes / Q000096:biosynthesis; D013601:T-Lymphocytes / Q000502:physiology; D006377:T-Lymphocytes, Helper-Inducer / Q000502:physiology
D000485:Allergens; D007132:Immunoglobulin Isotypes; D007073:Immunoglobulin E