特应性皮炎：免疫偏离、屏障功能障碍、IgE自身反应性及新疗法。
Atopic dermatitis: immune deviation, barrier dysfunction, IgE autoreactivity and new therapies.
作者信息
Furue Masutaka, Chiba Takahito, Tsuji Gaku, Ulzii Dugarmaa, Kido-Nakahara Makiko, Nakahara Takeshi, Kadono Takafumi
机构信息
Department of Dermatology, Kyushu University, Fukuoka, Japan; Research and Clinical Center for Yusho and Dioxin, Kyushu University, Fukuoka, Japan; Division of Skin Surface Sensing, Department of Dermatology, Kyushu University, Fukuoka, Japan.
Department of Dermatology, Kyushu University, Fukuoka, Japan.
出版信息
Allergol Int. 2017 Jul;66(3):398-403. doi: 10.1016/j.alit.2016.12.002. Epub 2017 Jan 2.
Atopic dermatitis (AD) is a chronic or chronically relapsing, eczematous, severely pruritic skin disorder mostly associated with IgE elevation and skin barrier dysfunction due to decreased filaggrin expression. The lesional skin of AD exhibits Th2- and Th22-deviated immune reactions that are progressive during disease chronicity. Th2 and Th22 cytokines further deteriorate the skin barrier by inhibiting filaggrin expression. Some IgEs are reactive to self-antigens. The IgE autoreactivity may precipitate the chronicity of AD. Upon activation of the ORAI1 calcium channel, atopic epidermis releases large amounts of thymic stromal lymphopoietin (TSLP), which initiates the Th2 and Th22 immune response. Th2-derived interleukin-31 and TSLP induce an itch sensation. Taken together, TSLP/Th2/Th22 pathway is a promising target for developing new therapeutics for AD. Enhancing filaggrin expression using ligands for the aryl hydrocarbon receptor may also be an adjunctive measure to restore the disrupted barrier function specifically for AD.
特应性皮炎（AD）是一种慢性或慢性复发性湿疹性、严重瘙痒性皮肤病，主要与由于丝聚合蛋白表达降低导致的IgE升高和皮肤屏障功能障碍有关。AD的皮损表现为Th2和Th22偏向的免疫反应，在疾病慢性期呈进行性发展。Th2和Th22细胞因子通过抑制丝聚合蛋白表达进一步损害皮肤屏障。一些IgE对自身抗原有反应。IgE自身反应性可能促使AD慢性化。特应性表皮激活ORAI1钙通道后会释放大量胸腺基质淋巴细胞生成素（TSLP），从而启动Th2和Th22免疫反应。Th2衍生的白细胞介素-31和TSLP会诱发瘙痒感。综上所述，TSLP/Th2/Th22通路是开发AD新疗法的一个有前景的靶点。使用芳烃受体配体增强丝聚合蛋白表达也可能是一种专门恢复AD受损屏障功能的辅助措施。
Zotero 插件