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Atopic dermatitis food allergens

A murine model of food-induced atopic dermatitis confirmed the important role of specific T cells in eczema here, C3H/HeJ mice were orally sensitized to cow s milk or peanut and thereafter exposed to the allergen. An eczematous eruption developed in approximately one third of mice after low-grade exposure to milk or peanut proteins. Histological examination of lesional skin revealed spongiosis and a cellular infiltrate mainly consisting of CD4-I- lymphocytes. [Pg.103]

Patients sensitized to pollen allergens often develop an IgE response to cross-reactive food allergens. Birch pollen-related food may lead to an exacerbation of eczema in a subpopulation of patients with atopic dermatitis and sensitization to birch pollen allergens. A birch pollen-specific T-cell response could be detected in lesional skin of these responding patients. T-cell cross-reactivity between Bet v 1 and related food allergens can occur independently of IgE cross-reactivity in vitro and in vivo. This has been shown in atopic dermatitis patients who developed late eczematous skin reactions to cooked food which was shown to elicit T-cell but not IgE-mediated responses [11]. [Pg.103]

Burks, A.W., Williams, L.W., Connaughton, C., Cockrell, G., O Brien, T.J., Helm, R.M. 1992. Allergenicity of peanut and soybean extracts altered by chemical or thermal denatur-ation in patients with atopic dermatitis and positive food challenges. J Allergy Clin Immunol 90 889-897. [Pg.289]

The duality of Thl and Th2 T-helper cells that exists in murine animals probably also exists in humans (14). It has been postulated that IL-4 enhancement promotes the development of IgE-mediated hypersensitivity disorders such as food allergy, while the combination of defective INF-y with enhanced IL-4 production promotes inflammatory atopic disorders such as atopic dermatitis and asthma. IgE irmnunoregulation suggests that the magnitude of the IgE response to persistent allergens depend upon this balance between T-helper cells and their cytokine production. However, environmental and other as yet unidentified factors also contribute to the allergic state of the predisposed individual. [Pg.355]

McFadden, J., White, J.M.L., Basketter, D., and Kimber, I. 2008. Reduced allergy rates in atopic eczema to contact allergens used in both skin products and foods Atopy and the hapten-atopy hypothesis. Contact Dermatitis 58(3) 156-158. [Pg.384]


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See also in sourсe #XX -- [ Pg.332 ]




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