Implications of IL-13Rα2 in atopic skin inflammation

Atopic dermatitis (AD) is a common eczematous skin disorder characterized by skin inflammation, barrier disruption, chronic pruritus and marked scratching. Th2 cytokines, especially IL-13, play a pathogenic role in AD. IL-13 signals via a heterodimeric receptor composed of IL-4R alpha and IL-13 R alpha 1. A second receptor, IL-13 R alpha 2, binds to IL-13 with high affinity, but it works as a decoy receptor. IL-13 R alpha 2 is overexpressed in the lesional skin of AD. Notably, mechanical scratching, as well as IL-13 itself, also upregulates IL-13 Rat expression. The scratch-induced IL-13 R alpha 2 upregulation may attenuate the IL-13-mediated epidermal barrier dysfunction and dermal fibrosis. Recent studies stress an importance of another IL-13 R alpha 2 ligand, chitinase 3-like 1 or YKL-40 in Th2 differentiation. However, the implications of increased IL-13 R alpha 2 levels remain elusive in AD. In this review, we summarize the recent topics on IL-13 R alpha 2 in atopic skin inflammation. Copyright (C) 2020, Japanese Society of Allergology. Production and hosting by Elsevier B.V.