Abstract
Dermatitis encompasses a spectrum of inflammatory skin disorders with aberrant immune responses classified as type 1, type 2, and/or type 3. Major advances in the understanding of the pathogenesis of atopic dermatitis (AD) have shed new light on how innate immune responses critically regulate type 2 inflammation and itch. This article highlights the diverse ways by which type 2 immune cells regulate diseases beyond AD. The discovery of human Mas-related G protein-coupled receptor X2 on mast cells has revealed novel Tcell-independent and immunoglobulin E-independent mechanisms of allergic contact dermatitis-associated and urticarial itch, respectively.
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