SLE-associated risk factors affect DC function.
SLE-associated risk factors affect DC function.
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DOI：
10.1111/imr.12348
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发表时间：
2016-01
影响因子：
8.7
通讯作者：
Diamond B
中科院分区：
文献类型：
--
作者：
Son M;Kim SJ;Diamond B
系统性红斑狼疮（SLE）的许多危险等位基因现已确定。对造血来源细胞中具有风险等位基因的基因表达的分析表明，它们在B细胞和树突状细胞（DC）中表达最丰富，这表明这些细胞类型可能是SLE中观察到的炎症变化的驱动因素。DC特别令人感兴趣，因为它们可以连接先天性免疫反应和适应性免疫反应。因此，DC可以将炎症转化为自身免疫，而自身抗体是SLE的标志。在这篇综述中，我们重点关注维持DC处于非活化、非免疫原性状态的耐受机制。我们证明，使用我们自己的研究中的例子，DC功能的改变源于DC-内在异常或DC-外在功能调节剂如何易患自身免疫。
Numerous risk alleles for systemic lupus erythematosus (SLE) have now been identified. Analysis of the expression of genes with risk alleles in cells of hematopoietic origin demonstrates them to be most abundantly expressed in B cells and dendritic cells (DCs), suggesting that these cell types may be the drivers of the inflammatory changes seen in SLE. DCs are of particular interest as they act to connect the innate and the adaptive immune response. Thus, DCs can transform inflammation into autoimmunity, and autoantibodies are the hallmark of SLE. In this review, we focus on mechanisms of tolerance that maintain DCs in a non‐activated, non‐immunogenic state. We demonstrate, using examples from our own studies, how alterations in DC function stemming from either DC‐intrinsic abnormalities or DC‐extrinsic regulators of function can predispose to autoimmunity.