Kawasaki disease, a systemic vasculitis that affects young children and can result in coronary artery aneurysms, is the leading cause of acquired heart disease among children. A hallmark of Kawasaki disease is increased blood platelet counts and platelet activation, which is associated with an increased risk of developing resistance to intravenous immunoglobulin and coronary artery aneurysms. Platelets and their releasate, including granules, microparticles, microRNAs and transcription factors, can influence innate immunity, enhance inflammation and contribute to vascular remodelling. Growing evidence indicates that platelets also interact with immune and non-immune cells to regulate inflammation. Platelets boost NLRP3 inflammasome activation and IL-1β production by human immune cells by releasing soluble mediators. Activated platelets form aggregates with leukocytes, such as monocytes and neutrophils, enhancing numerous functions of these cells and promoting thrombosis and inflammation. Leukocyte–platelet aggregates are increased in children with Kawasaki disease during the acute phase of the disease and can be used as biomarkers for disease severity. Here we review the role of platelets in Kawasaki disease and discuss progress in understanding the immune-effector role of platelets in amplifying inflammation related to Kawasaki disease vasculitis and therapeutic strategies targeting platelets or platelet-derived molecules.

川崎病是一种影响幼儿并可导致冠状动脉瘤的系统性血管炎，是儿童获得性心脏病的主要原因。川崎病的一个标志是血小板计数和血小板活化增加，这与对静脉注射免疫球蛋白和冠状动脉瘤产生抵抗力的风险增加有关。血小板及其释放物，包括颗粒、微粒、微小RNA和转录因子，可以影响先天免疫、增强炎症并有助于血管重塑。越来越多的证据表明血小板还与免疫和非免疫细胞相互作用来调节炎症。血小板通过释放可溶性介质来促进 NLRP3 炎性体激活和人类免疫细胞产生 IL-1β。活化的血小板与单核细胞和中性粒细胞等白细胞形成聚集体，增强这些细胞的多种功能并促进血栓形成和炎症。患有川崎病的儿童在疾病急性期白细胞-血小板聚集体增加，可用作疾病严重程度的生物标志物。在这里，我们回顾血小板在川崎病中的作用，并讨论了解血小板在放大川崎病血管炎相关炎症中的免疫效应器作用的进展，以及针对血小板或血小板衍生分子的治疗策略。