Evidence map›Paper›PMID 31354729›Full record

ReviewFrontiers in immunology2019

The Human Platelet as an Innate Immune Cell: Interactions Between Activated Platelets and the Complement System.

Oskar Eriksson, Camilla Mohlin, Bo Nilsson, Kristina N Ekdahl

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
12.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

88 citing papers in PubMed, 137 citations in OpenAlex.

  1. Accumulation of amyloid beta in human glioblastomas.Clinical and experimental immunology · 2020
    Trial
  2. Article
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  5. Review
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  8. Complement system in tumor growth and metastases.British journal of cancer · 2026
    Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. A Novel Role for Platelet-Endothelial Crosstalk in Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2025
    Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Article

28 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Oskar ErikssonDepartment of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.
Camilla MohlinLinnaeus Center of Biomaterials Chemistry, Linnaeus University, Kalmar, Sweden.
Bo NilssonDepartment of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.
Kristina N EkdahlDepartment of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.
Uppsala University · SELinnaeus University · SE

Funding

Swedish Research Council
6 · The paper itself

Abstract

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.

Indexed as

Blood PlateletsCell CommunicationComplement ActivationComplement Membrane Attack ComplexHumansImmunity, InnatePlatelet ActivationThrombocytopeniaComplement Membrane Attack Complexcomplementdisulfidesinnate immunitylectin pathwayphosphorylationplateletsthiol isomerases

Identifiers

PMID31354729
PMCPMC6635567
OpenAlexW2961930484

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.