tetano
Editor, Senior Moderator
Front Immunol
. 2023 May 19;14:1186000.
doi: 10.3389/fimmu.2023.1186000. eCollection 2023. Platelet-neutrophil interaction in COVID-19 and vaccine-induced thrombotic thrombocytopenia
Johannes Hirsch[SUP] 1 2 [/SUP], Günalp Uzun[SUP] 1 2 [/SUP], Jan Zlamal[SUP] 1 2 [/SUP], Anurag Singh[SUP] 1 [/SUP], Tamam Bakchoul[SUP] 1 2 [/SUP]
Affiliations
Coronavirus disease 2019 (COVID-19) is known to commonly induce a thrombotic diathesis, particularly in severely affected individuals. So far, this COVID-19-associated coagulopathy (CAC) has been partially explained by hyperactivated platelets as well as by the prothrombotic effects of neutrophil extracellular traps (NETs) released from neutrophils. However, precise insight into the bidirectional relationship between platelets and neutrophils in the pathophysiology of CAC still lags behind. Vaccine-induced thrombotic thrombocytopenia (VITT) is a rare autoimmune disorder caused by auto-antibody formation in response to immunization with adenoviral vector vaccines. VITT is associated with life-threatening thromboembolic events and thus, high fatality rates. Our concept of the thrombophilia observed in VITT is relatively new, hence a better understanding could help in the management of such patients with the potential to also prevent VITT. In this review we aim to summarize the current knowledge on platelet-neutrophil interplay in COVID-19 and VITT.
Keywords: COVID-19; VITT; coagulopathy; immunothrombosis; neutrophil extracellular traps (NET); platelet activation.
. 2023 May 19;14:1186000.
doi: 10.3389/fimmu.2023.1186000. eCollection 2023. Platelet-neutrophil interaction in COVID-19 and vaccine-induced thrombotic thrombocytopenia
Johannes Hirsch[SUP] 1 2 [/SUP], Günalp Uzun[SUP] 1 2 [/SUP], Jan Zlamal[SUP] 1 2 [/SUP], Anurag Singh[SUP] 1 [/SUP], Tamam Bakchoul[SUP] 1 2 [/SUP]
Affiliations
- PMID: 37275917
- PMCID: PMC10237318
- DOI: 10.3389/fimmu.2023.1186000
Coronavirus disease 2019 (COVID-19) is known to commonly induce a thrombotic diathesis, particularly in severely affected individuals. So far, this COVID-19-associated coagulopathy (CAC) has been partially explained by hyperactivated platelets as well as by the prothrombotic effects of neutrophil extracellular traps (NETs) released from neutrophils. However, precise insight into the bidirectional relationship between platelets and neutrophils in the pathophysiology of CAC still lags behind. Vaccine-induced thrombotic thrombocytopenia (VITT) is a rare autoimmune disorder caused by auto-antibody formation in response to immunization with adenoviral vector vaccines. VITT is associated with life-threatening thromboembolic events and thus, high fatality rates. Our concept of the thrombophilia observed in VITT is relatively new, hence a better understanding could help in the management of such patients with the potential to also prevent VITT. In this review we aim to summarize the current knowledge on platelet-neutrophil interplay in COVID-19 and VITT.
Keywords: COVID-19; VITT; coagulopathy; immunothrombosis; neutrophil extracellular traps (NET); platelet activation.