Role of interferons in SLE

被引：101

作者：

Bengtsson, Anders A. ^{[1
]}

Ronnblom, Lars ^{[2
]}

机构：

[1] Lund Univ, Skdne Univ Hosp, Dept Clin Sci Lund, Rheumatol, S-22185 Lund, Sweden

[2] Uppsala Univ, Sect Rheumatol, Sci Life Lab, Dept Med Sci, SE-75185 Uppsala, Sweden

来源：

BEST PRACTICE & RESEARCH IN CLINICAL RHEUMATOLOGY | 2017年 / 31卷 / 03期

基金：

瑞典研究理事会;

关键词：

Lupus erythematosus; systemic; Interferon type I; Plasmacytoid dendritic cell; Biologic therapy; SYSTEMIC-LUPUS-ERYTHEMATOSUS; PLASMACYTOID DENDRITIC CELLS; IFN-ALPHA PRODUCTION; NEUTROPHIL EXTRACELLULAR TRAPS; CONTAINING IMMUNE-COMPLEXES; I-INTERFERON; MONOCLONAL-ANTIBODY; C1Q DEFICIENCY; RISK HAPLOTYPE; MURINE LUPUS;

D O I：

10.1016/j.berh.2017.10.003

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease that affects many different organ systems, with excessive production of type I interferons (IFNs) and auto antibodies against nucleic acids as hallmarks. Activation of the type I IFN system in SLE is due to continuous stimulation of plasmacytoid dendritic cells by endogenous nucleic acids, leading to sustained type I IFN production. This is reflected by an over expression of type I IFN-regulated genes or an IFN signature. Type I IFNs have effects on both the innate and adaptive immune systems, which contribute to both loss of tolerance and the autoimmune disease process. In this review, we discuss the current understanding of IFNs in SLE, focusing on their regulation, the influence of genetic background, and environmental factors and therapies that are under development aiming to inhibit the type I IFN system in SLE. (C) 2017 Elsevier Ltd. All rights reserved.

引用

页码：415 / 428

页数：14

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