Crosstalk between platelets and the complement system in immune protection and disease

Verschoor, Admar; Langer, Harald F.

doi:10.1160/th13-02-0102

Cited by 78 publications

(31 citation statements)

References 120 publications

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“…There is emerging evidence that the activation of complement receptors on platelets may be of pathophysiological relevance in certain diseases such as atypical haemolytic uraemic syndrome (aHUS) [42]. Our results point in the same direction for patients with CAD as we found that in the prothrombotic environment in ACS patients, the up-regulation of anaphylatoxin receptors C3aR and C5aR on platelets correlates with platelet activation markers such as SDF-1 and P-selectin.…”

Section: Discussionsupporting

confidence: 80%

Expression of anaphylatoxin receptors on platelets in patients with coronary heart disease

et al. 2015

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Section: Discussionsupporting

confidence: 80%

Expression of anaphylatoxin receptors on platelets in patients with coronary heart disease

et al. 2015

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“…Complement proteins also interact with bacteria both through the conventional pathway and the alternative pathway (53, 54). S. sanguinis for example induces platelet aggregation involving complement (55).…”

Section: Platelets and Bacterial Infectionsmentioning

confidence: 99%

Platelets and Infections â€“ Complex Interactions with Bacteria

et al. 2015

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Platelets can be considered sentinels of vascular system due to their high number in the circulation and to the range of functional immunoreceptors they express. Platelets express a wide range of potential bacterial receptors, including complement receptors, FcγRII, Toll-like receptors but also integrins conventionally described in the hemostatic response, such as GPIIb–IIIa or GPIb. Bacteria bind these receptors either directly, or indirectly via fibrinogen, fibronectin, the first complement C1q, the von Willebrand Factor, etc. The fate of platelet-bound bacteria is questioned. Several studies reported the ability of activated platelets to internalize bacteria such as Staphylococcus aureus or Porphyromonas gingivalis, though there is no clue on what happens thereafter. Are they sheltered from the immune system in the cytoplasm of platelets or are they lysed? Indeed, while the presence of phagolysosome has not been demonstrated in platelets, they contain antimicrobial peptides that were shown to be efficient on S. aureus. Besides, the fact that bacteria can bind to platelets via receptors involved in hemostasis suggests that they may induce aggregation; this has indeed been described for Streptococcus sanguinis, S. epidermidis, or C. pneumoniae. On the other hand, platelets are able to display an inflammatory response to an infectious triggering. We, and others, have shown that platelet release soluble immunomodulatory factors upon stimulation by bacterial components. Moreover, interactions between bacteria and platelets are not limited to only these two partners. Indeed, platelets are also essential for the formation of neutrophil extracellular traps by neutrophils, resulting in bacterial clearance by trapping bacteria and concentrating antibacterial factors but in enhancing thrombosis. In conclusion, the platelet–bacteria interplay is a complex game; its fine analysis is complicated by the fact that the inflammatory component adds to the aggregation response.

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“…This physiological intervention and repair are no less than a healing process, which itself relates to physiological inflammation. To assist this physiological inflammation, platelets produce assortments of repair tools, such as clotting factors, cytokines, and other BRMs, growth factors, and angiogenic factors ( 23 , 35 , 75 , 104 – 108 ). Apart from taht, platelets can surpass their physiological role and participate in pathological inflammation, as with cardiovascular disease, severe infection and sepsis, and arthritis ( 18 , 23 , 29 , 31 , 32 , 36 , 75 , 105 , 106 , 109 – 117 ).…”

Section: Platelets As Immune Cellsmentioning

confidence: 99%

Are Platelets Cells? And if Yes, are They Immune Cells?

2015

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Small fragments circulating in the blood were formally identified by the end of the nineteenth century, and it was suggested that they assisted coagulation via interactions with vessel endothelia. Wright, at the beginning of the twentieth century, identified their bone-marrow origin. For long, platelets have been considered sticky assistants of hemostasis and pollutants of blood or tissue samples; they were just cell fragments. As such, however, they were acknowledged as immunizing (to specific HPA and HLA markers): the platelet’s dark face. The enlightened face showed that besides hemostasis, platelets contained factors involved in healing. As early as 1930s, platelets entered the arsenal of medicines were transfused, and were soon manipulated to become a kind of glue to repair damaged tissues. Some gladly categorized platelets as cells but they were certainly not fully licensed as such for cell physiologists. Actually, platelets possess almost every characteristic of cells, apart from being capable of organizing their genes: they have neither a nucleus nor genes. This view prevailed until it became evident that platelets play a role in homeostasis and interact with cells other than with vascular endothelial cells; then began the era of physiological and also pathological inflammation. Platelets have now entered the field of immunity as inflammatory cells. Does assistance to immune cells itself suffice to license a cell as an “immune cell”? Platelets prove capable of sensing different types of signals and organizing an appropriate response. Many cells can do that. However, platelets can use a complete signalosome (apart from the last transcription step, though it is likely that this step can be circumvented by retrotranscribing RNA messages). The question has also arisen as to whether platelets can present antigen via their abundantly expressed MHC class I molecules. In combination, these properties argue in favor of allowing platelets the title of immune cells.

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Crosstalk between platelets and the complement system in immune protection and disease

Cited by 78 publications

References 120 publications

Expression of anaphylatoxin receptors on platelets in patients with coronary heart disease

Expression of anaphylatoxin receptors on platelets in patients with coronary heart disease

Platelets and Infections â€“ Complex Interactions with Bacteria

Are Platelets Cells? And if Yes, are They Immune Cells?

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