炎症体
血小板
先天免疫系统
细胞生物学
血小板活化
炎症
免疫学
生物
半胱氨酸蛋白酶1
化学
免疫系统
作者
Verena Rolfes,Lucas S. Ribeiro,Ibrahim Hawwari,Lisa Böttcher,Nathalia Rosero,Salie Maasewerd,Marina Lima Silva Santos,Tomasz Próchnicki,Camila Meirelles de Souza Silva,Carlos Wagner de Souza Wanderley,Maximilian Rothe,Susanne V. Schmidt,H. James Stunden,Damien Bertheloot,Magali Noval Rivas,Cor Jésus Fernandes Fontes,Luzia H. Carvalho,Fernando Q. Cunha,Eicke Latz,Moshe Arditi,Bernardo S. Franklin
出处
期刊:Cell Reports
[Elsevier]
日期:2020-05-01
卷期号:31 (6): 107615-107615
被引量:88
标识
DOI:10.1016/j.celrep.2020.107615
摘要
The inflammasomes control the bioactivity of pro-inflammatory cytokines of the interleukin (IL)-1 family. The inflammasome assembled by NLRP3 has been predominantly studied in homogeneous cell populations in vitro, neglecting the influence of cellular interactions that occur in vivo. Here, we show that platelets boost the inflammasome capacity of human macrophages and neutrophils and are critical for IL-1 production by monocytes. Platelets license NLRP3 transcription, thereby enhancing ASC oligomerization, caspase-1 activity, and IL-1β secretion. Platelets influence IL-1β production in vivo, and blood platelet counts correlate with plasmatic IL-1β levels in malaria. Furthermore, we reveal an enriched platelet gene signature among the highest-expressed transcripts in IL-1β-driven autoinflammatory diseases. The platelet effect is independent of cell-to-cell contact, platelet-derived lipid mediators, purines, nucleic acids, and a host of platelet cytokines, and it involves the triggering of calcium-sensing receptors on macrophages. Hence, platelets provide an additional layer of regulation of inflammasomes and IL-1-driven inflammation.
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