Systemic lupus erythematosus(SLE),also known as type Ⅰ IFN 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 type ⅠIFN.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 type Ⅰ IFN abnormality in patients.Regulating the overactive immune response and the overexpression of type Ⅰ IFN play important roles in alleviating the disease.Autophagy,as an important process regula-ting body homeostasis,can inhibit the type Ⅰ IFN response.In this review,we discuss how the selective autophagic receptors tripartite motif 21(TRIM21),stimulator of interferon genes(STING),and p62 affect type Ⅰ IFN response by mediating auto-phagy of key regulators in multiple pathways.
维普
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