The cytokine thymic stromal lymphopoietin (TSLP) has recently been implicated in the pathogenesis of atopic dermatitis (AD) and other allergic diseases in humans. To further characterize its role in this disease process, transgenic mice were generated that express a keratinocyte-specific, tetracycline-inducible TSLP transgene. Skin-specific overexpression of TSLP resulted in an AD-like phenotype, with the development of eczematous lesions containing inflammatory dermal cellular infiltrates, a dramatic increase in Th2 CD4 T cells expressing cutaneous homing receptors, and elevated serum levels of IgE. These transgenic mice demonstrate that TSLP can initiate a cascade of allergic inflammation in the skin and provide a valuable animal model for future study of this common disease.

Atopic dermatitis (AD) is a common allergic inflammatory disease of the skin that is characterized by intense pruritus and chronic eczematous plaques and is often associated with a personal or family history of allergic disease (1, 2). In addition, it is the most common chronic skin disease in childhood, affecting an estimated 7–12% of school-aged children (3). Although most cases are mild and usually clear up, some patients experience severe or widespread disease that can be physically, socially, and/or emotionally debilitating (4). Although the underlying cause of AD remains unclear, its pathogenesis is thought to involve a Th2 cell–mediated allergic inflammatory cascade (5, 6). This type of inflammation is characterized by the production of proallergic cytokines (IL-4, IL-5, IL-13, and TNF-) by CD4 T cells, leading to elevated levels of IgE and leukocytic infiltration of the dermis (6, 7). Local DCs are thought to play a crucial role in this process by polarizing naive CD4 T cells to differentiate into Th2 lymphocytes. However, the initiating factors that influence these impor-