角质形成细胞与2型炎症互作在特应性皮炎发病机制中的作用  

The role of interaction between keratinocytes and type 2 inflammation in the pathogenesis of atopic dermatitis

作　　者：张睿文 黄小宝 王芳[1] ZHANG Ruiwen;HUANG Xiaobao;WANG Fang(First Affiliated Hospital,Sun Yat-sen University,Guangzhou 510080,China)

机构地区：[1]中山大学附属第一医院,广东广州510080

出　　处：《皮肤性病诊疗学杂志》2024年第1期48-55,共8页Journal of Diagnosis and Therapy on Dermato-venereology

基　　金：国家自然科学基金(82273511);国家自然科学基金委员会中德科学中心中德合作交流项目(M-0747);广东省自然科学基金(2022B1515020067);中山大学创新人才培育计划项目(22ykqb03)。

摘　　要：特应性皮炎(AD)患者皮肤屏障功能受损,与角质形成细胞(KC)异常密切相关。在外界因素的刺激下,KC释放炎症因子、趋化因子等炎症介质,作用于2型免疫细胞,进而引起皮肤免疫向2型炎症方向偏移。反之,2型炎症进一步加剧皮肤屏障破坏,故而形成恶性循环。因此,KC和2型炎症之间的互作是促进AD发生发展、加剧炎症反应与瘙痒的重要因素。目前,AD治疗领域的靶向创新药物如生物制剂和小分子药的抗炎作用已逐步得到证实,部分研究表明他们还具有修复皮肤屏障的作用。针对KC与2型炎症互作的研究不仅有助于理解AD的发病机制,也有望优化疾病的治疗方案,提供更多治疗参考。Patients with atopic dermatitis(AD)have skin barrier dysfunction,which is closely related to keratinocyte(KC)abnormalities.Upon stimulation by external factors,KCs release a large number of inflammatory mediators,thereby activating type 2 inflammation,which,in turn,exacerbates skin barrier dysfunction.Thus,the interaction between KCs and type 2 inflammation is a key factor in the pathogenesis of AD,and exacerbation of inflammation and pruritus.At present,the innovative medications,such as biologics and small molecule drugs,have been shown anti-inflammatory effects in AD.Studies also demonstrate their role in skin barrier repair.Therefore,research on the interaction between KCs and type 2 inflammation will help understand the pathogenesis of AD and provide evidence to optimize treatment strategies for AD.

关 键 词：特应性皮炎 角质形成细胞 2型炎症 生物制剂 小分子药 

分 类 号：R758.2[医药卫生—皮肤病学与性病学]