2018
Platelets kill bacteria by bridging innate and adaptive immunity via platelet factor 4 and FcγRIIA
Abstract: Background Activated platelets release the chemokine platelet factor 4 (PF4) stored in their granules. PF4 binds to polyanions (P) on bacteria, undergoes a conformational change and exposes neoepitopes. These neoepitopes induce production of anti-PF4/P antibodies. As PF4 binds to a variety of bacteria, anti-PF4/P IgG can bind and opsonize several bacterial species. Objective Here we investigated whether platelets are able to kill bacteria directly after recognizing anti-PF4/P IgG opsonized bacteria in the pres…
Search citation statements
Paper Sections
Select...
72
13
13
2
Citation Types
3
88
2
2
Year Published
2018
2026
Publication Types
Select...
81
6
6
1
Relationship
3
91
Authors
Journals
Cited by 93 publications
(95 citation statements)
References 53 publications
3
88
2
2
“…However, C3a, RANTES and PF4 concentrations were found to increase in RT-stored components, which aligns with previous reports [7,21,44]. PF4 and C3a are involved in anti-pathogen responses [26,45], while RANTES has been linked to a higher risk of adverse transfusion events [43].…”
Section: Discussionsupporting
confidence: 90%
“…However, C3a, RANTES and PF4 concentrations were found to increase in RT-stored components, which aligns with previous reports [7,21,44]. PF4 and C3a are involved in anti-pathogen responses [26,45], while RANTES has been linked to a higher risk of adverse transfusion events [43].…”
Section: Discussionsupporting
confidence: 90%
“…However, C3a, RANTES and PF4 concentrations were found to increase in RT‐stored components, which aligns with previous reports [7,21,44]. PF4 and C3a are involved in anti‐pathogen responses [26,45], while RANTES has been linked to a higher risk of adverse transfusion events [43]. Further, cold‐stored platelets exhibited a lower abundance of several key leukocyte adhesion (HCAM, ICAM‐2) and co‐stimulatory (B7‐2, DC‐SIGN, CD40) receptors.…”
Section: Discussionsupporting
confidence: 87%
“… 15 This was suggested to be due to QD interaction with GPIIb/IIIa. This is similar to the proposed mechanism of action for platelets binding to bacteria, resulting in bacteria localisation to the centre of platelets close to organelles, in which GPIIb/IIa has a large role, 42 which allows for spatial regulation of granule secretion, 43 potentially towards the QD. Further research is needed to fully understand how and why QDs interact, and what the specific effect on the platelet is when that interaction occurs.…”
Section: Discussionsupporting
confidence: 70%
“…In the present study, native E. coli bacterial strains did not trigger measurable killing by platelets . Therefore, it seems that the long stretches of LPS found on native bacteria are so long that they hide the Fc part of the IgG (i.e.…”
Section: The Fcγriia and Platelet–bacteria Interactionscontrasting
confidence: 53%
“…In the present study, native E. coli bacterial strains did not trigger measurable killing by platelets [1]. Therefore, it seems that the long stretches of LPS found on native Formation of PF4-heparin neo-epitopes results in heparin-induced thrombocytopenia PF4 can also bind to negatively charged molecules, such as exogenous heparin and endogenous heparin-like molecules present on endothelial cells, exposing similar PF4/anion neo-epitopes that can be recognized by circulating anti-PF4 IgGs.…”
Section: The Role Of Platelets In Bacterial Infections: What About Thcontrasting
confidence: 46%
