Epidermal TSLP: a trigger factor for pathogenesis of atopic dermatitis

Abstract

Atopic dermatitis (AD) is a common allergic inflammatory skin disease that affects 10–20% of infants, besides 3–5% of adults, and is often linked with family history of allergic disease [1]. It is characterized by strong itchy and inflamed skin and chronic lichenified, more scaly plaques. AD, asthma and allergic rhinitis forms an “atopic triad” and share a common pathogenesis, involving a T helper type 2 (Th2) cell–mediated allergic inflammation. This inflammation is characterized by secretion of cytokines (IL-4, IL-5, IL-13, and TNFα) by CD4+ T-cells, which trigger increased IgE antibody-production by B-cells; IgE binding to mast cells facilitates initiation of allergic reactions and drives infiltration of leucocytes into the skin dermis {[2], and refs therein}. Homing dendritic cells (DCs) control polarization of naive CD4+ T-cells to differentiate into Th2 lymphocytes. However, the initiating factor(s) that influence these important antigen-presenting cells to instruct T-helper cell polarization toward this inflammatory phenotype, and the mechanisms underlying the preferential activation of Th2-cells in atopic individuals by external allergens is poorly understood.