Atopic dermatitis cell-mediated reactions

Atopic dermatitis has been proposed to be the cutaneous manifestation of IgE-mediated hypersensitive reaction to allergenic substances [29]. Conceptually, antagonizing IgE emerges as a logical therapeutic option. Systemic treatment with omalizumab, however, appears to be less efficacious in the skin than in the airway mucosa [23]. It is possible that small molecule Syk inhibitors may offer a more suitable mode to reach and prevent activation of sensitized dermal mast cells and dendritic cells. 

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]. 

This chapter will review our current knowledge about the pathogenesis of allergic skin disorders, in particular atopic dermatitis (AD) and urticaria. Anti-lgE therapy has not been systematically studied in these skin diseases. Therefore we will discuss the role of IgE in their pathogenesis and provide a scientific rationale for use of anti-IgE treatment in these diseases. Recent studies indicate that the IgE molecule has a multifunctional role in these diseases, acting as both a target and a key player in the elicitation of allergen-induced immediate hypersensitivity reactions and cell-mediated responses. 

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