Food allergy

Department of Pediatrics, Mount Sinai School of Medicine, New York, New York, USA.
Current opinion in gastroenterology (Impact Factor: 4.29). 11/2011; 28(2):99-103. DOI: 10.1097/MOG.0b013e32834e7b60
Source: PubMed


How food protein becomes recognized as an allergen remains a fundamental question. Previous studies indicated that the pathophysiology of food allergy is because of a skewed Th2 response to specific food glycoproteins. The focus has now shifted to understanding how a failure of regulatory mechanisms results in food allergy. This review summarizes the recent findings elucidating the small intestine's role in the pathophysiology of food allergy and the immune mechanisms of oral tolerance.
Gut homeostasis and immunity occur via a complex interplay of innate and adaptive immune responses. Immune exclusion is performed mainly by secretory IgA, although there are back-up mechanisms in place to induce oral tolerance when secretory IgA is lacking. Oral tolerance cannot occur in murine models lacking T regulatory cells, for which Foxp3+ is a key marker. Migration of Foxp3+ T cells from the mesenteric lymph nodes (MLNs) to the lamina propria occurs via gut-homing signals. Also in the MLNs are CD103+ dendritic cells, which drive the differentiation of Foxp3+ T cells in the presence of TGF-β and retinoic acid produced from dietary vitamin A. Lastly, microenvironmental signals from the microbiome can serve to enhance these interactions.
We have focused primarily on local immunologic variables that may affect the induction of oral tolerance in the gut and the mechanisms elucidated in animal models. However, many other variables such as genetics, commensal microbiota, and diet are likely to be important factors.

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