Food allergy is an adverse reaction to dietary antigens that results from a breakdown of immune tolerance to ingested foods. The prevalence of food allergy has risen dramatically in the last few decades. Food allergy has significant morbidity, dramatically impairs quality of life, and creates a tremendous burden on our healthcare system. Although important advances have been made in understanding the breakdown of tolerance and the resultant reactions to food antigens, many aspects of the deviation of the immune response causing food allergy remain unclear. The involvement of IgE and increased T helper 2 (Th2) immune responses in these patients indicate that defects in adaptive immunity are part of the pathogenesis of food allergy. However, non-IgE-mediated food allergy disorders such eosinophilic esophagitis (EoE), a chronic allergic disease characterized by excessive accumulation of eosinophils in the esophagus, indicate that additional pathways also participate in adverse reactions to food antigens. This suggests that the cells involved are often not part of the adaptive immune system. In addition, a number of genetic and environmental factors that predispose to food allergy and EoE implicate innate cells in the allergic diathesis, including epithelial cells and innate immune cells . Despite current advances, the underlying causes of inappropriate activation and regulation of the innate immune system in food allergy and EoE remain poorly understood.

Given the growing evidence that changes in innate immune function contribute to the pathogenesis of food allergy, the goal of this Research Topic is to provide insight into the role of innate immune cells in the development of food allergy and EoE. This issue will focus on functional alterations of gastrointestinal mucosal and submucosal cells with emphasis on molecular, cellular, and intercellular mechanisms leading to increased sensitization/uptake of food allergens, increased number or activity of effector cells critical in allergic immune responses and inflammatory pathways.

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Media Contact:

Kathy Andrews
Journal Manager
Journal of Clinical & Experimental Dermatology Research
Email: derma@peerreviewedjournals.com