Implications of IL-13Rα2 in atopic skin inflammation

Allergology International

Gaku Tsuji¹  Dugarmaa Ulzii²  Makiko Kido-Nakahara²  Takeshi Nakahara³  Masutaka Furue⁴  Kazuhisa Furue⁴  Akiko Hashimoto-Hachiya⁴ 

[1] Corresponding author. Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka, 812-8582, Japan.;Division of Skin Surface Sensing, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan;Research and Clinical Center for Yusho and Dioxin, Kyushu University Hospital, Fukuoka, Japan;Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan;

关键词: IL-13Rα2;    IL-13;    Atopic dermatitis;    Scratch;    YKL-40;   

DOI  :  

来源: DOAJ

【 摘 要 】

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-4Rα and IL-13 Rα1. A second receptor, IL-13 Rα2, binds to IL-13 with high affinity, but it works as a decoy receptor. IL-13 Rα2 is overexpressed in the lesional skin of AD. Notably, mechanical scratching, as well as IL-13 itself, also upregulates IL-13 Rα2 expression. The scratch-induced IL-13 Rα2 upregulation may attenuate the IL-13-mediated epidermal barrier dysfunction and dermal fibrosis. Recent studies stress an importance of another IL-13 Rα2 ligand, chitinase 3-like 1 or YKL-40 in Th2 differentiation. However, the implications of increased IL-13 Rα2 levels remain elusive in AD. In this review, we summarize the recent topics on IL-13 Rα2 in atopic skin inflammation.

【 授权许可】

Unknown