Platelet activation and neutrophil extracellular trap (NET) formation in immune thrombocytopenia: is there an association?

Lozano, María Luisa; Garabet, Lamya; Fernández-Pérez, María Piedad; Reyes-García, Ascensión M. de los; Diaz-Lozano, Pedro; García-Barberá, Nuria; Águila, Sonia; Vicente, Vicente; Martı́nez, Constantino; Gónzález-Conejero, Rocío

doi:10.1080/09537104.2019.1696456

Cited by 10 publications

(19 citation statements)

References 46 publications

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“…APS is a systemic disease characterized by thrombotic or obstetrical events, with thrombocytopenia 1 . Neutrophil activation and extracellular neutrophil traps are likely involved in antiphospholipid antibody associated thrombosis and thrombophilia 2,3 . We find platelet phagocytesis by neutrophils in this patient, which suggests that neutrophil activation may contribute to the pathogenesis of APS.…”

Section: Figurementioning

confidence: 56%

Platelet phagocytosis by neutrophils in a patient with antiphospholipid syndrome

Zhang

2021

Rheumatology & Autoimmunity

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Section: Figurementioning

confidence: 56%

Platelet phagocytosis by neutrophils in a patient with antiphospholipid syndrome

Zhang

2021

Rheumatology & Autoimmunity

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“…(Table 3). In fact, the presence of the abovementioned NETs has been described in patients suffering from arterial (acute coronary syndrome, coronary artery disease, and stroke) and venous (deep vein thrombosis, pulmonary embolism) thrombotic episodes, and other related syndromes (thrombocytopenia, septic shock with disseminated intravascular coagulation, Behçet's disease, Cushing disease) [150,[177][178][179][180][181][182][183][184][185][186][187][188][189][190][191][192][193][194][195]. These clinical studies correlated a specific molecular pattern of the NETs with the severity of tissue damage using parameters and signs, such as infarct size, stenosis grade, electrocardiogram disturbances, stroke scores, thrombus stabilization and growth, thrombin potential ratio, tronponin T peak, hypercoagulability markers, protein C reactive, and glucose levels (Table 3).…”

Section: Figurementioning

confidence: 99%

The Neutrophil Secretome as a Crucial Link between Inflammation and Thrombosis

Blanch-Ruiz

Ortega-Luna

Martínez-Cuesta

et al. 2021

IJMS

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Cardiovascular diseases are a leading cause of death. Blood–cell interactions and endothelial dysfunction are fundamental in thrombus formation, and so further knowledge of the pathways involved in such cellular crosstalk could lead to new therapeutical approaches. Neutrophils are secretory cells that release well-known soluble inflammatory signaling mediators and other complex cellular structures whose role is not fully understood. Studies have reported that neutrophil extracellular vesicles (EVs) and neutrophil extracellular traps (NETs) contribute to thrombosis. The objective of this review is to study the role of EVs and NETs as key factors in the transition from inflammation to thrombosis. The neutrophil secretome can promote thrombosis due to the presence of different factors in the EVs bilayer that can trigger blood clotting, and to the release of soluble mediators that induce platelet activation or aggregation. On the other hand, one of the main pathways by which NETs induce thrombosis is through the creation of a scaffold to which platelets and other blood cells adhere. In this context, platelet activation has been associated with the induction of NETs release. Hence, the structure and composition of EVs and NETs, as well as the feedback mechanism between the two processes that causes pathological thrombus formation, require exhaustive analysis to clarify their role in thrombosis.

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“…So far, however, conflicting results have been published about platelet activation in ITP. Platelet activation has been reported to be either increased, within normal range or decreased in ITP [19][20][21]. Platelet activation, rather than platelet counts, has been suggested to be a possible predictor of bleeding risk [21][22][23].…”

Section: Platelet Activation and Immune Functionsmentioning

confidence: 99%

“…NETs are web-like chromatin complexes that are released by neutrophils in the circulation upon activation [27]. NETs are able to trap pathogens and elicit antimicrobial and inflammatory properties [19,27,28]. Aberrant NET formation (NETosis) has been described to propagate inflammation in various autoimmune diseases such as RA, SLE and anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis [19,28].…”

Section: Platelets and Inflammation In Itpmentioning

confidence: 99%

“…NETs are able to trap pathogens and elicit antimicrobial and inflammatory properties [19,27,28]. Aberrant NET formation (NETosis) has been described to propagate inflammation in various autoimmune diseases such as RA, SLE and anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis [19,28]. It has been speculated, for example, that NET formation can stimulate dendritic cells and autoreactive B cells in a TLR-9 dependent manner in patients with small vessel vasculitis [28].…”

Section: Platelets and Inflammation In Itpmentioning

confidence: 99%

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Platelets in ITP: Victims in Charge of Their Own Fate?

Nelson

Jolink

Amini

et al. 2021

Cells

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Immune thrombocytopenia (ITP) is an autoimmune bleeding disorder. The pathophysiological mechanisms leading to low platelet levels in ITP have not been resolved, but at least involve autoantibody-dependent and/or cytotoxic T cell mediated platelet clearance and impaired megakaryopoiesis. In addition, T cell imbalances involving T regulatory cells (Tregs) also appear to play an important role. Intriguingly, over the past years it has become evident that platelets not only mediate hemostasis, but are able to modulate inflammatory and immunological processes upon activation. Platelets, therefore, might play an immuno-modulatory role in the pathogenesis and pathophysiology of ITP. In this respect, we propose several possible pathways in which platelets themselves may participate in the immune response in ITP. First, we will elaborate on how platelets might directly promote inflammation or stimulate immune responses in ITP. Second, we will discuss two ways in which platelet microparticles (PMPs) might contribute to the disrupted immune balance and impaired thrombopoiesis by megakaryocytes in ITP. Importantly, from these insights, new starting points for further research and for the design of potential future therapies for ITP can be envisioned.

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Platelet activation and neutrophil extracellular trap (NET) formation in immune thrombocytopenia: is there an association?

Cited by 10 publications

References 46 publications

Platelet phagocytosis by neutrophils in a patient with antiphospholipid syndrome

Platelet phagocytosis by neutrophils in a patient with antiphospholipid syndrome

The Neutrophil Secretome as a Crucial Link between Inflammation and Thrombosis

Platelets in ITP: Victims in Charge of Their Own Fate?

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