Neutrophils in the pathogenesis and manifestations of SLE.
Neutrophils in the pathogenesis and manifestations of SLE.
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DOI：
10.1038/nrrheum.2011.132
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发表时间：
2011-09-27
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影响因子：
--
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系统性红斑狼疮(SLE)是一种病因不明的自身免疫性疾病，主要影响育龄妇女。遗传和环境因素引起的先天性免疫和获得性免疫功能异常在系统性红斑狼疮的发病机制中起重要作用。尽管如此，中性粒细胞--最丰富的免疫细胞类型--在这种疾病的病理中的作用尚不清楚。在过去的十年里，有令人信服的证据表明，中性粒细胞与系统性红斑狼疮的启动和持续存在有关，也与这种疾病患者经常观察到的器官损害有关。SLE来源的低密度粒细胞(LDGs)可诱导血管损伤和合成数量增加的I型干扰素，因此可能在SLE的发病机制中发挥重要作用。此外，在SLE患者中性粒细胞中观察到的细胞死亡增加和细胞外陷阱形成增加可能在SLE患者自身免疫的诱导和器官损害的发生中起关键作用。总而言之，这些事件可能会产生显著的有害影响，并促进这种疾病的异常免疫反应。本文着重介绍了中性粒细胞在系统性红斑狼疮发病机制中的作用，并着重介绍了低密度脂蛋白和中性粒细胞胞外陷阱的可能有害作用。
Systemic lupus erythematosus (SLE) is an autoimmune disease of unclear etiology that affects mostly women of childbearing age. Profound abnormalities in both innate and adaptive immunity triggered by genetic and environmental factors are well documented to play an important part in the pathogenesis of SLE. Nonetheless, the role of neutrophils—the most abundant immune cell type—in the pathology of this disease has been unclear. Over the past decade, compelling evidence has emerged that implicates neutrophils in the initiation and perpetuation of SLE and also in the resultant organ damage frequently observed in patients with this disease. SLE-derived low-density granulocytes (LDGs) induce vascular damage and synthesize increased amounts of type I interferons and, as such, could play a prominent part in the pathogenesis of SLE. Furthermore, increased cell death and enhanced extracellular trap formation observed in SLE-derived neutrophils might have key roles in the induction of autoimmunity and the development of organ damage in patients with SLE. Together, these events could have significant deleterious effects and promote aberrant immune responses in this disease. This Review highlights the role of neutrophils in the pathogenesis of SLE, with a particular focus on the putative deleterious effects of LDGs and neutrophil extracellular trap formation.
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影响因子：
5.5
作者：
ARVIEUX, J;JACOB, MC;COLOMB, MG
通讯作者：
COLOMB, MG
影响因子：
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作者：
ABRAMSON, SB;GIVEN, WP;WEISSMANN, G
通讯作者：
WEISSMANN, G
影响因子：
--
作者：
AMOURA, Z;CHABRE, H;JACOB, L
通讯作者：
JACOB, L
影响因子：
27.4
作者：
Cairns, AP;Crockard, AD;Bell, AL
通讯作者：
Bell, AL
DOI：
10.1084/jem.20021553
发表时间：
2003-03-17
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Bennett L;Palucka AK;Arce E;Cantrell V;Borvak J;Banchereau J;Pascual V
通讯作者：
Pascual V