NLRP3炎症小体在特应性皮炎中的调控机制及治疗应用OA
Regulatory mechanism and therapeutic application of NLRP3 inflammasome in atopic dermatitis
特应性皮炎是一种由遗传、免疫及环境因素共同导致的慢性炎症性皮肤病,具有持续性和复发性特征.核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)炎症小体通过多种刺激物激活后促进炎性细胞因子白细胞介素(IL)-1β和IL-18成熟,进而调节辅助性 T 淋巴细胞(Th)2/Th1免疫偏移,在特应性皮炎急性期和慢性期的发病过程中发挥关键作用,抑制其活化可显著减轻特应性皮炎的症状.本综述系统总结了NLRP3炎症小体在特应性皮炎中的致病机制及治疗应用的研究进展,为靶向NLRP3炎症小体的抑制剂应用于特应性皮炎治疗提供了理论基础.
Atopic dermatitis(AD)is a chronic inflammatory skin disease caused by genetic,immunological and environmental factors,with persistent and recurrent characteristics.Nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)inflammasome promotes the maturation of inflammatory factors interleukin(IL)-1β and IL-18 through the activation of various stimuli,and then regulate the helper-T lymphocytes(Th)2/Th1 immune shift,which plays a key role in the pathogenesis of atopic dermatitis in acute and chronic phases.Inhibition of its activation can significantly alleviate symptoms of AD.This review systematically summarizes the research progress in the pathogenesis and therapeutic applications of the NLRP3 inflammasome in AD,which provides a theoretical basis for the application of inhibitors targeting this inflammasome for the treatment of atopic dermatitis.
梁书宁;金珊
延边大学附属医院皮肤科,吉林 延吉 133000延边大学附属医院皮肤科,吉林 延吉 133000
医药卫生
特应性皮炎炎症小体核苷酸结合寡聚化结构域样受体蛋白3抑制剂
atopic dermatitisinflammasomenucleotide-binding oligomerization domain-like receptor protein 3inhibitor
《中国医科大学学报》 2026 (4)
372-376,5
国家自然科学基金(82060573)
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