选择性自噬受体对SLE患者Ⅰ型IFN过表达调节的研究进展  

Research progress on the regulation of typeⅠIFN overexpression by selective autophagy receptors in SLE patients

作　　者：孙平 魏正萍 付萍[1] SUN Ping;WEI Zheng-ping;FU Ping(Department of Rheumatology and Clinical Immunology,the Second Affiliated Hospital of Kunming Medical University,Kunming 650101,China)

机构地区：[1]昆明医科大学第二附属医院风湿免疫科,昆明650101

出　　处：《现代免疫学》2024年第1期61-64,71,共5页Current Immunology

基　　金：国家自然科学基金(81860287);昆明医科大学2022年研究生创新基金(2022S269)。

摘　　要：系统性红斑狼疮(systemic lupus erythematosus,SLE)也被称为Ⅰ型IFN特征性疾病,是一种病因不明的慢性全身性自身免疫性疾病。体内过度免疫应答和Ⅰ型IFN的过量表达为该病的主要特征。在固有免疫应答过程中,核酸感受器对于病原体及体内核酸的过度反应是导致患者体内Ⅰ型IFN异常的主要原因之一。调节体内过度免疫反应及Ⅰ型IFN的过量表达对于缓解病情有重要作用。自噬作为调控机体稳态的重要过程可以抑制Ⅰ型IFN应答。该文就选择性自噬受体三方基序蛋白21(tripartite motif 21,TRIM21)、干扰素基因刺激物(stimulator of interferon gene,STING)、p62通过介导多种信号通路中的关键调节因子的自噬来影响Ⅰ型IFN应答展开探讨。Systemic lupus erythematosus(SLE),also known as typeⅠIFN signature disease,is a chronic systemic autoimmune disease of unknown etiology.The main features of the disease are the overactive immune response and overexpression of typeⅠIFN.In the course of innate immune response,the overactive immune reaction of nucleic acid receptor to pathogen and nucleic acid in vivo is one of the reasons that lead to the typeⅠIFN abnormality in patients.Regulating the overactive immune response and the overexpression of typeⅠIFN play important roles in alleviating the disease.Autophagy,as an important process regulating body homeostasis,can inhibit the typeⅠIFN response.In this review,we discuss how the selective autophagic receptors tripartite motif 21(TRIM21),stimulator of interferon genes(STING),and p62 affect typeⅠIFN response by mediating autophagy of key regulators in multiple pathways.

关 键 词：系统性红斑狼疮 Ⅰ型干扰素 自噬受体 

分 类 号：R593.241[医药卫生—内科学]