By Novartis Foundation symposium on Anaphylaxis
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Extra info for Anaphylaxis
Human Th2 cytokines (interleukins 4 and 13) induce co-expression of IgE and IgG4 through sequential switching. The regulation of IgG4 responses and the role of these responses in the pathogenesis of allergy have not been characterized. We are addressing these issues by comparing and contrasting the expression of allergen-speci¢c IgE and IgG4 in a population of European children thoroughly de¢ned for lifestyle, environmental exposures and allergic phenotypes. The current analysis focused exclusively on children from non-farming families (n ¼ 493) in order to avoid potential e¡ects of exposure to microbial products abundant in farming environments.
Of patients that are referred to us that have been given treatment for anaphylaxis, over half have been misdiagnosed. For example, I do my anaesthetic reaction clinic with an experienced consultant anaesthetist, and in two-thirds of cases referred following a ‘reaction’ we ¢nd an alternative cause for the event and no evidence for anaphylaxis. Galli: In these cases are the patients presenting with the clinical picture of anaphylaxis because of mast cell activation by a non-immunological mechanism, or do they have something else entirely?
This discrepancy may result from di¡erences between the immunization routes, target organs, and regulatory networks engaged in these conditions. Furthermore, inhalant and parasite-derived Th2 ANTIBODIES AND ALLERGY 35 allergens are likely to di¡er in their biochemical structure and the biological context within which they are presented to the immune system. We conclude by proposing a model for the generation of allergen-speci¢c antibody responses predicated on our current results (Fig. 3). Allergen-speci¢c, Th2-mediated antibody responses represent the outcome of two fundamental choices made by a developing CD4+ Th cell precursor.
Anaphylaxis by Novartis Foundation symposium on Anaphylaxis