EADV 2026视频特辑｜Christopher Bunick教授：特应性皮炎：屏障与免疫互作及长期疾病修饰

Christopher Bunick教授系统阐述了特应性皮炎（AD）治疗理念的演进。他结合 LEVEL UP 头对头试验生物标志物分析，阐述 AD 中屏障与免疫的双向互作：乌帕替尼的作用不局限于 Th2 炎症，还可下调 Th1、Th17、Th22，并上调丝聚蛋白2、兜甲蛋白与晚期角化包膜蛋白等屏障蛋白。基于 Measure Up 1 和 2 研究公布的 140 周数据，他提出以"最小疾病活动度"再定义长期治疗成功，并展望分子层面的疾病修饰与全身性炎症管理。

Assoc. Prof. Christopher Bunick gave a systematic account of the evolution of treatment concepts in atopic dermatitis (AD). Drawing on biomarker analyses from the head-to-head LEVEL UP trial, he explained the bidirectional crosstalk between the skin barrier and immunity in AD: upadacitinib acts beyond Th2 inflammation, also downregulating Th1, Th17 and Th22 while upregulating barrier proteins such as filaggrin-2, loricrin and late cornified envelope proteins. Based on the 140-week data from the Measure Up 1 and 2 studies, he proposed redefining long-term treatment success in terms of "minimal disease activity," and looked ahead to disease modification at the molecular level and the management of systemic inflammatory.