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The Human Platelet as an Innate Immune Cell: Interactions Between Activated Platelets and the Complement System
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
Linnaeus Univ, Linnaeus Ctr Biomat Chem, Kalmar, Sweden.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.ORCID iD: 0000-0003-0057-2730
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology. Linnaeus Univ, Linnaeus Ctr Biomat Chem, Kalmar, Sweden.ORCID iD: 0000-0001-7888-1571
2019 (English)In: Frontiers in Immunology, ISSN 1664-3224, E-ISSN 1664-3224, Vol. 10, article id 1590Article, review/survey (Refereed) Published
Abstract [en]

Platelets play an essential role in maintaining homeostasis in the circulatory system after an injury by forming a platelet thrombus, but they also occupy a central node in the intravascular innate immune system. This concept is supported by their extensive interactions with immune cells and the cascade systems of the blood. In this review we discuss the close relationship between platelets and the complement system and the role of these interactions during thromboinflammation. Platelets are protected from complement-mediated damage by soluble and membrane-expressed complement regulators, but they bind several complement components on their surfaces and trigger complement activation in the fluid phase. Furthermore, localized complement activation may enhance the procoagulant responses of platelets through the generation of procoagulant microparticles by insertion of sublytic amounts of C5b9 into the platelet membrane. We also highlight the role of post-translational protein modifications in regulating the complement system and the critical role of platelets in driving these reactions. In particular, modification of disulfide bonds by thiol isomerases and protein phosphorylation by extracellular kinases have emerged as important mechanisms to fine-tune complement activity in the platelet microenvironment. Lastly, we describe disorders with perturbed complement activation where part of the clinical presentation includes uncontrolled platelet activation that results in thrombocytopenia, and illustrate how complement-targeting drugs are alleviating the prothrombotic phenotype in these patients. Based on these clinical observations, we discuss the role of limited complement activation in enhancing platelet activation and consider how these drugs may provide opportunities for further dissecting the complex interactions between complement and platelets.

Place, publisher, year, edition, pages
Frontiers Media S.A., 2019. Vol. 10, article id 1590
Keywords [en]
complement, platelets, lectin pathway, disulfides, phosphorylation, thiol isomerases, innate immunity
National Category
Immunology in the medical area Immunology
Identifiers
URN: urn:nbn:se:uu:diva-390426DOI: 10.3389/fimmu.2019.01590ISI: 000474774200001PubMedID: 31354729OAI: oai:DiVA.org:uu-390426DiVA, id: diva2:1342039
Funder
Swedish Research Council, 2015-06429Swedish Research Council, 2016-2075-5.1Swedish Research Council, 2016-04519Available from: 2019-08-12 Created: 2019-08-12 Last updated: 2019-08-12Bibliographically approved

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