Pubblicazioni

Impaired pro‐resolving mechanisms promote abnormal NETosis , fueling autoimmunity in sickle cell disease  (2023)

Autori:
Recchiuti, Antonio; Federti, Enrica; Matte', Alessandro; Mazzi, Filippo; Ceolan, Jacopo; Porreca, Annamaria; Di Nicola, Marta; Menotti, Sofia; Alivernini, Stefano; DE FRANCESCHI, Lucia
Titolo:
Impaired pro‐resolving mechanisms promote abnormal NETosis , fueling autoimmunity in sickle cell disease
Anno:
2023
Tipologia prodotto:
Articolo in Rivista
Tipologia ANVUR:
Articolo su rivista
Lingua:
Inglese
Formato:
A Stampa
Referee:
Nome rivista:
American Journal of Hematology
ISSN Rivista:
0361-8609
N° Volume:
98
Numero o Fascicolo:
3
Intervallo pagine:
E45-E48
Parole chiave:
neptosis, sickle cell disease, immunity
Breve descrizione dei contenuti:
Sickle cell disease (SCD) is a worldwide distributed hereditary red cell disorders with still high mortality and morbidity and limited therapeutic options. SCD is characterized by anemia, chronic hemolysis, and acute vaso-occlusive painful crises. The biocomplexity of SCD goes beyond red cells, involving neutrophils and soluble factors such as cytokines or alternative complement pathway intensively cross-talking with vascular endothelial cells. In addition, in SCD, the overactivation of neutrophils contributes to the production of neutrophil extracellular traps (NETs) (1, 2). This might trigger endothelial vascular injury, promoting acute sickle cell related events and increasing the risk of infections in patients with SCD
Id prodotto:
133163
Handle IRIS:
11562/1090250
ultima modifica:
30 ottobre 2024
Citazione bibliografica:
Recchiuti, Antonio; Federti, Enrica; Matte', Alessandro; Mazzi, Filippo; Ceolan, Jacopo; Porreca, Annamaria; Di Nicola, Marta; Menotti, Sofia; Alivernini, Stefano; DE FRANCESCHI, Lucia, Impaired pro‐resolving mechanisms promote abnormal NETosis , fueling autoimmunity in sickle cell disease «American Journal of Hematology» , vol. 98 , n. 32023pp. E45-E48

Consulta la scheda completa presente nel repository istituzionale della Ricerca di Ateneo IRIS

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