Atopic dermatitis (AD) is a common inflammatory skin disease resulting from epidermal barrier dysfunction and an immune response dominated by IL-4-producing Th2 cells and IL-22-producing Th22 cells. Environmental antigens like food allergens are thought to influence the clinical course of AD. We aimed to study the pathogenic phenotype of food allergen-specific T cells activated through the skin or by oral exposure and their potency to transfer skin inflammation. Ovalbumin (OVA) TCR-transgenic mice were sensitized epicutaneously with OVA or were fed OVA. CD4+ T cells from skin or mesenteric lymph nodes were phenotyped for cytokine expression and transferred into naïve BALB/c mice. Recipient mice were challenged with OVA epicutaneously. Skin inflammation was determined histologically. T cells activated through epicutaneous or oral OVA exposure in donor mice both migrate to skin lymph nodes after adoptive transfer and epicutaenous OVA exposure of recipient mice. Importantly, AD-like skin inflammation could only be induced by the transfer of epicutaneously primed OVA T cells. Analysis of the immune phenotype demonstrated an IL-22/IL-17A-dominated immune phenotype of skin-pathogenic T cells. IL-22 seems to be the critical cytokine for the development of AD and is induced in this model by epicutaneous sensitization with OVA.

Epicutaneous allergen exposure induces pathogenic IL-22-producing T helper cells