Service de Rhumatologie, FHU ACRONIM, Hôpital Pellegrin, Centre Hospitalier Universitaire, place Amélie Raba Léon, 33076, Bordeaux, France.
Université de Bordeaux, 146 rue Léo Saignat, 33076, Bordeaux, France.
Curr Rheumatol Rep. 2017 Aug;19(8):48. doi: 10.1007/s11926-017-0678-0.
Current knowledge on the role of platelets and platelet-derived microparticles (PMPs) on the immune system has been fast-growing. Systemic lupus erythematosus (SLE) is a systemic auto-immune disorder characterized by a loss of tolerance toward nuclear auto-antigens. Although recent studies allowed a better understanding of SLE pathogenesis, there is an urgent need for the development of new treatments and the identification of new biomarkers to assess the disease activity. We describe here the state-of-the-art knowledge linking platelets and PMPs to SLE.
Platelet system activation is a key event in the pathogenesis of SLE. Circulating immune complexes, anti-phospholipid antibodies, and infectious agents such as virus are the main activators of platelets in SLE. Platelet activation can be monitored through different ways such as P-selectin expression, mean platelet volume, or circulating PMP levels, suggesting their potential use as biomarkers. Upon activation, platelets promote type I interferon production, NETosis, dendritic cell activation, and T and B lymphocyte activation, all essential events contributing to the development of SLE. Of interest, platelets also play a fundamental role in SLE organ disease such as the development of cardiovascular, thrombotic, and renal diseases. Finally, we review current knowledge on drugs targeting platelet activation and their potential impact on SLE pathogenesis. Platelets play a major role in SLE pathogenesis and organ disease and represent a great potential for novel biomarkers and drug development.
目前，关于血小板和血小板衍生的微颗粒（PMP）在免疫系统中的作用的知识正在迅速增长。系统性红斑狼疮（SLE）是一种全身性自身免疫性疾病，其特征是对核自身抗原的耐受性丧失。尽管最近的研究使人们对 SLE 的发病机制有了更好的理解，但仍迫切需要开发新的治疗方法和识别新的生物标志物来评估疾病活动。我们在这里描述了将血小板和 PMP 与 SLE 联系起来的最新知识。
血小板系统的激活是 SLE 发病机制中的一个关键事件。循环免疫复合物、抗磷脂抗体和感染因子（如病毒）是 SLE 中血小板的主要激活剂。血小板的激活可以通过不同的方式来监测，如 P-选择素表达、平均血小板体积或循环 PMP 水平，这表明它们具有作为生物标志物的潜在用途。血小板激活后，可促进 I 型干扰素的产生、NETosis、树突状细胞的激活以及 T 和 B 淋巴细胞的激活，所有这些都是导致 SLE 发展的重要事件。有趣的是，血小板在 SLE 的器官疾病中也起着至关重要的作用，如心血管疾病、血栓形成和肾脏疾病的发展。最后，我们综述了目前针对血小板激活的药物及其对 SLE 发病机制的潜在影响的知识。血小板在 SLE 的发病机制和器官疾病中起着重要作用，为新型生物标志物和药物开发提供了巨大的潜力。
