婴幼儿特应性皮炎的皮肤屏障、瘙痒与Th2型免疫相关性

Correlation of skin barrier,itching and Th2 type immune in infantile atopic dermatitis

特应性皮炎(atopic dermatitis,AD)是一种表现为皮肤反复瘙痒的慢性疾病。皮肤屏障功能不完善、皮肤瘙痒与辅助型T细胞2型免疫失调是婴幼儿AD发生及发展过程中的重要疾病特征,三者相辅相成、互为因果。婴幼儿皮肤屏障尚未完全形成,其皮肤容易受到病原体和毒素等刺激物入侵,从而引发自身免疫调节失衡,如辅助型T细胞2型细胞因子的激活。该免疫失衡会进一步降低皮肤屏障相关蛋白(如丝聚蛋白、角蛋白等)的表达,加剧皮肤屏障受损。另外,刺激物的侵入会激活激肽释放酶,通过蛋白酶激活受体2途径传导瘙痒感觉,导致患者不断抓挠皮肤,形成“屏障不全-免疫紊乱-瘙痒-抓挠-屏障受损”致病循环。本文根据国内外AD研究现状,从皮肤屏障功能、瘙痒机制与辅助型T细胞2型免疫失调三个方面阐述了婴幼儿AD发病机理,重点分析了由于屏障功能发育不全导致婴幼儿AD的发生机制,总结了当前AD干预措施及未来可能的研究方向,以期为婴幼儿AD相关药物以及护肤品的研发提供理论依据和新思路。

Atopic dermatitis(AD)is a chronic ailment characterized by recurrent skin pruritus.Imperfections in the skin barrier,itchiness,and dysregulation of Th2 immunity are important features that interplay and perpetuate the disease in infants and young children.The incomplete formation of the skin barrier in infants leaves their epidermis susceptible to invasion by pathogens,toxins and irritants,which triggers an imbalance in autoimmune regulation,for example,activation of Th2 cytokines which further decreases the expression of skin barrier-associated proteins such as filaggrin and keratins,exacerbating skin barrier damage.Additionally,the intrusion of irritants triggers the activation of kallikreins,which transduces itch sensation through the protease-activated receptor 2 pathway,instigating a cycle of scratching by the patient,which results in a vicious cycle of“barrier defect-immune dysregulation-itch-scratching-barrier damage”,perpetuating the disease.Grounded in the current state of AD research both domestically and internationally,this work elucidates the pathogenesis of AD in infants from three perspectives:skin barrier function,itch mechanism and Th2 immune dysregulation;scrutinizes the mechanism by which the incomplete development of the barrier function leads to AD in infants;summarizes current AD interventions and forecasts potential future directions,aiming to provide a theoretical foundation and novel insights for the development of medication and skincare products for infants with AD.