Characterizing novel genes and pathways in the pathogenesis of IgE food allergies

[Truncated abstract] The prevalence of IgE-mediated food allergies and adverse reactions to foods has risen dramatically over the past 15 years, particularly in Australia, the UK, and North America. This has been most apparent in infants and very young children, placing substantial pressure on health services and significant burden on the children, their families and educational systems. As with other allergic conditions, the rise in food allergy appears to be the consequence of increasingly urbanised environments and 'modern lifestyles', adversely affecting the immune system early in development. Despite the pressing need to elucidate this, neither the pathogenesis nor the causal pathways of food allergy have been clearly defined. Previous studies suggest that food allergy is associated with a failure of regulatory mechanisms that normally suppress the emergence of CD4+ Th2 cells, thereby allowing the production of excessive allergen-specific IgE. Importantly, pre-symptomatic differences in immune function are detectable at birth in children who develop IgE-mediated food allergies, suggesting that the immune dysregulation is initiated in utero. Elucidation of the specific early differences in gene expression patterns in allergic individuals may provide valuable clues to both pathogenesis of food allergy and pathways susceptible to environmental influence.