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首页> 外文期刊>Cytokine >Coordination between innate immune cells, type I IFNs and IRF5 drives SLE pathogenesis
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Coordination between innate immune cells, type I IFNs and IRF5 drives SLE pathogenesis

机译：先天免疫细胞之间的协调，I型IFNS和IRF5驱动SLE发病机制

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摘要

Systemic lupus erythematosus (SLE) is a complex autoimmune disease which affects multiple organs. The type I interferon (IFN) gene signature and circulating autoantibodies are hallmarks of SLE. Plasmacytoid dendritic cells (pDCs) are considered the main producers of type I IFN and production is modulated by multiple other immune cell types. In SLE, essentially every immune cell type is dysregulated and aberrant deregulation is thought to be due, in part, to direct or indirect exposure to IFN. Genetic variants within or around the transcription factor interferon regulatory factor 5 (IRF5) associate with SLE risk. Elevated IFN alpha activity was detected in the sera of SLE patients carrying IRF5 risk polymorphisms who were positive for either anti-RNA binding protein (anti-RBP) or anti-double-stranded DNA (anti-dsDNA) autoantibodies. Neutrophils are also an important source of type I IFNs and are found in abundance in human blood. Neutrophil extracellular traps (NETs) are considered a potential source of antigenic trigger in SLE that can lead to type I IFN gene induction, as well as increased autoantibody production. In this review, we will focus on immune cell types that produce type I IFNs and/or are affected by type I IFN in SLE. In addition, we will discuss potential inducers of endogenous type I IFN production in SLE. Last, we will postulate how the different immune cell populations may be affected by an IRF5-SLE risk haplotype.
机译：Systemic Lupus红斑（SLE）是一种复杂的自身免疫疾病，影响多个器官。 I型Interferon（IFN）基因签名和循环自身抗体是SLE的标志。血浆胸泡树突细胞（PDC）被认为是I I型IFN和生产的主要生产商由多种其他免疫细胞类型调节。在SLE中，基本上，每种免疫细胞类型都被引起了测定，并且认为是由于直接或间接暴露于IFN的异常放松管制。转录因子干扰素调节因子5（IRF5）内或周围的遗传变异与SLE风险相关联。在携带IRF5患者的SLE患者的血清中检测到IFNα活性升高，所述IRF5风险多态性为抗RNA结合蛋白（抗RBP）或抗双链DNA（抗DSDNA）自身抗体。嗜中性粒细胞也是I I型IFNS的重要来源，并且在人类血液中被发现。中性粒细胞细胞外疏水阀（网）被认为是SLE中的抗原触发的潜在来源，其可以导致I IFN基因诱导，以及增加的自身抗体产生。在本综述中，我们将专注于产生I型IFNS和/或受到SLE中类型IFN的影响的免疫细胞类型。此外，我们将讨论SLE中内源性I IFN生产的潜在诱导剂。最后，我们将假定不同免疫细胞种群的影响可能受IRF5-SLE风险单倍型的影响。

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