Platelet Factor 4 and Duffy Antigen Required for Platelet Killing of
            <i>Plasmodium falciparum</i>

McMorran, Brendan J.; Wieczorski, Laura; Drysdale, Karen E.; Chan, Jo‐Anne; Huang, Huiyan; Smith, Clare M.; Mitiku, Chalachew; Beeson, James G.; Burgio, Gaétan; Foote, Simon J.

doi:10.1126/science.1228892

Cited by 156 publications

(168 citation statements)

References 33 publications

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“…Upon detection of infection, activated platelets bind to infected red blood cells and induce directed a-granule release [28]. One of the soluble mediators released in this response is platelet factor 4 (PF4), a CXC-type chemokine that inhibits parasite growth and kills the pathogen [28]. Interestingly, PF4 has also been shown to bind to the Duffy-antigen receptor (Fy), resulting in the death of infected red blood cells [28].…”

Section: Direct Pathogen Killingmentioning

confidence: 99%

“…One of the soluble mediators released in this response is platelet factor 4 (PF4), a CXC-type chemokine that inhibits parasite growth and kills the pathogen [28]. Interestingly, PF4 has also been shown to bind to the Duffy-antigen receptor (Fy), resulting in the death of infected red blood cells [28]. Moreover, human platelets, upon activation, release b-defensins that have direct and potent antimicrobial effects on Staphylococcus aureus [11].…”

Section: Direct Pathogen Killingmentioning

confidence: 99%

“…Recent work on the causative parasite of malaria, Plasmodium falciparum, has identified a unique mechanism whereby platelets can contribute directly to pathogen killing. Upon detection of infection, activated platelets bind to infected red blood cells and induce directed a-granule release [28]. One of the soluble mediators released in this response is platelet factor 4 (PF4), a CXC-type chemokine that inhibits parasite growth and kills the pathogen [28].…”

Section: Direct Pathogen Killingmentioning

confidence: 99%

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Platelets: bridging hemostasis, inflammation, and immunity

Jenne

Urrutia

Kubes

2013

Int J Lab Hematology

317

264

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Summary Although the function of platelets in the maintenance of hemostasis has been studied in great detail, more recent evidence has highlighted a central role for platelets in the host inflammatory and immune responses. Platelets by virtue of their large numbers and their ability to rapidly release a broad spectrum of immunomodulatory cytokines, chemokines, and other mediators act as circulating sentinels. Upon detection of a pathogen, platelets quickly activate and begin to drive the ensuing inflammatory response. Platelets have the ability to directly modulate the activity of neutrophils (phagocytosis, oxidative burst), endothelium (adhesion molecule and chemokine expression), and lymphocytes. Due to their diverse array of adhesion molecules and preformed chemokines, platelets are able to adhere to leukocytes and facilitate their recruitment to sites of tissue damage or infection. Furthermore, platelets directly participate in the capture and sequestration of pathogens within the vasculature. Platelet–neutrophil interactions are known to induce the release of neutrophil extracellular traps (NETs) in response to either bacterial or viral infection, and platelets have been shown to internalize pathogens, sequestering them in engulfment vacuoles. Finally, emerging data indicate that platelets also participate in the host immune response by directly killing infected cells. This review will highlight the central role platelets play in the initiation and modulation of the host inflammatory and immune responses.

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Section: Direct Pathogen Killingmentioning

confidence: 99%

Section: Direct Pathogen Killingmentioning

confidence: 99%

Section: Direct Pathogen Killingmentioning

confidence: 99%

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Platelets: bridging hemostasis, inflammation, and immunity

Jenne

Urrutia

Kubes

2013

Int J Lab Hematology

317

264

View full text Add to dashboard Cite

show abstract

“…Besides its role on pathology, CXCL4 also participates in parasite clearance in early stages of the infection [24]. This is in the harmony with the recently discovered fact that platelets participate in early protective phases during malaria, which suggests that reduction in the count of platelets or the CXCL4 neutralization cannot be considered as a therapeutic measure.…”

Section: Platelet -Specific Cytokines and Cerebral Malariamentioning

confidence: 75%

Role of Platelet-Mediated Cytoadherence and Chemokines Release in Severe Malaria

Srivastava¹

2015

SOJI

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“…falciparum interaction with platelets might also lead to platelet activation and release of inflammatory mediators (Srivastava et al, 2008;McMorran et al, 2009;McMorran et al, 2012) however, the precise role of platelets in malaria pathology remains unclear. The assessment of P. falciparum clumping is affected by the precise conditions used to set up the clumping assay in vitro, with parasitaemia and haematocrit having a profound effect on the outcome of the assay.…”

Section: Platelet-mediated Clumping Assaymentioning

confidence: 99%

Platelet-mediated clumping adhesion phenotypes of P. falciparum-infected erythrocytes: A review

Onyambu¹,

Tanui²,

Alwala³

et al. 2017

Clin. Rev. Opinions

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Malaria is a leading cause of morbidity and mortality in the world. In general, malaria is easily treated but in a subset of cases it develops to severe disease. Severe malaria has a high rate of mortality even with the best available care. This creates the need for intensive research to fully characterise the pathogenesis of the disease in order to create future novel therapies. One of the hallmarks of malaria infections is its ability to adhere to specific sites in the body leading to severe disease syndromes such as cerebral malaria and pregnancy associated malaria. In this review, the platelet-mediated clumping adhesion phenotypes of malaria-infected erythrocytes were discussed in the context of infected erythrocyte adhesion phenotypes such as cytoadhesion and rosetting. Platelet-mediated clumping refers to a phenomenon of P. falciparum-infected erythrocytes whereby they agglutinate to form large aggregates held together by activated platelets. This unique phenotype is important because it has been associated with severe malaria in both children and adults in diverse geographical and transmission settings. The precise mechanisms by which platelet-mediated clumping occurs are yet to be precisely described. The platelet receptors implicated in this phenotype include CD36, P-Selectin and gC1qR. The parasite derived ligands that mediate this phenotype are yet to be described.

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Platelet Factor 4 and Duffy Antigen Required for Platelet Killing of Plasmodium falciparum

Cited by 156 publications

References 33 publications

Platelets: bridging hemostasis, inflammation, and immunity

Platelets: bridging hemostasis, inflammation, and immunity

Role of Platelet-Mediated Cytoadherence and Chemokines Release in Severe Malaria

Platelet-mediated clumping adhesion phenotypes of P. falciparum-infected erythrocytes: A review

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