Along with all allergic diseases, the prevalence of food
allergies has increased markedly in recent decades in industrialized nations.
An estimated 5% of children and up to 4% of adults are living with food allergy
and the fear of having a life threatening allergic reaction. Incidentally,
atopic dermatitis (AD) is a known risk factor for developing food allergies
later in life. However, the mechanisms through which antigen sensitization in
the skin can predispose to allergic inflammation in the intestine remain
unclear. Considering AD skin lesions are associated with elevated thymic
stromal lymphopoietin (TSLP) expression and basophil infiltration, Noti et al
determined that TSLP-elicited basophils promote antigen-induced intestinal food
allergy (J Allergy Clin Immunol 2014; 133(5): 1390-99).
The authors employed
a new model of food allergy by sensitizing mice to food antigens on an AD-like
skin lesion that predisposed to allergic inflammation in the intestine upon
oral antigen feeding. Oral antigen exposure of skin-sensitized mice resulted in
antigen specific IgE responses, type-2 inflammation and the accumulation of
mast cells in the intestine. In addition to intestinal food allergy, mice also
developed eosinophilic esophagitis (EoE)-like disease, a food allergy related
disorder. They determined that antigen-induced food allergy is dependent on
TSLP that elicits basophils to promote antigen-specific Th2 cytokine responses.
Furthermore, the authors demonstrate that TSLP-elicited basophils are both
necessary and sufficient to promote IgE-mediated intestinal food allergy in their
model.
Despite the challenges associated with mouse models, Noti
and colleagues have provided significant insight into mechanisms that mediate
food allergy by using a novel animal
model that mimics some characteristics of human disease. Targeting the TSLP-basophil axis may offer a
novel therapeutic approach to treatment and prevention of food allergy.
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