Autophagy is a homeostatic process responsible for the self-digestion of intracellular components and antimicrobial defense by inducing the degradation of pathogens into autophagolysosomes. Recent findings suggest an involvement of this process in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. However, the role of autophagy in the immunological mechanisms of coronavirus disease 2019 (COVID-19) pathogenesis remains largely unexplored. This study reveals the presence of autophagy defects in peripheral immune cells from COVID-19 patients. The impairment of the autophagy process resulted in a higher percentage of lymphocytes undergoing apoptosis in COVID-19 patients. Moreover, the inverse correlation between autophagy markers levels and peripheral lymphocyte counts in COVID-19 patients confirms how a defect in autophagy might contribute to lymphopenia, causing a reduction in the activation of viral defense. These results provided intriguing data that could help in understanding the cellular underlying mechanisms in COVID-19 infection, especially in severe forms.

Autophagy hijacking in PBMC From COVID-19 patients results in lymphopenia / Barbati, Cristiana; Celia, Alessandra Ida; Colasanti, Tania; Vomero, Marta; Speziali, Mariangela; Putro, Erisa; Buoncuore, Giorgia; Savino, Flavia; Colafrancesco, Serena; Ucci, Federica Maria; Ciancarella, Claudia; Balbinot, Eugenia; Scarpa, Susanna; Natalucci, Francesco; Pellegrino, Greta; Ceccarelli, Fulvia; Spinelli, Francesca Romana; Mastroianni, Claudio Maria; Conti, Fabrizio; Alessandri, Cristiano. - In: FRONTIERS IN IMMUNOLOGY. - ISSN 1664-3224. - 13:(2022). [10.3389/fimmu.2022.903498]

Autophagy hijacking in PBMC From COVID-19 patients results in lymphopenia

Barbati, Cristiana
;
Celia, Alessandra Ida;Colasanti, Tania;Vomero, Marta;Speziali, Mariangela;Putro, Erisa;Buoncuore, Giorgia;Colafrancesco, Serena;Ucci, Federica Maria;Ciancarella, Claudia;Balbinot, Eugenia;Scarpa, Susanna;Natalucci, Francesco;Pellegrino, Greta;Ceccarelli, Fulvia;Spinelli, Francesca Romana;Mastroianni, Claudio Maria;Conti, Fabrizio;Alessandri, Cristiano
2022

Abstract

Autophagy is a homeostatic process responsible for the self-digestion of intracellular components and antimicrobial defense by inducing the degradation of pathogens into autophagolysosomes. Recent findings suggest an involvement of this process in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. However, the role of autophagy in the immunological mechanisms of coronavirus disease 2019 (COVID-19) pathogenesis remains largely unexplored. This study reveals the presence of autophagy defects in peripheral immune cells from COVID-19 patients. The impairment of the autophagy process resulted in a higher percentage of lymphocytes undergoing apoptosis in COVID-19 patients. Moreover, the inverse correlation between autophagy markers levels and peripheral lymphocyte counts in COVID-19 patients confirms how a defect in autophagy might contribute to lymphopenia, causing a reduction in the activation of viral defense. These results provided intriguing data that could help in understanding the cellular underlying mechanisms in COVID-19 infection, especially in severe forms.
2022
COVID-19; SARS-CoV-2; apoptosis; autophagy; inflammation; lymphocytes; autophagy; humans; leukocytes, mononuclear; SARS-CoV-2; COVID-19; lymphopenia
01 Pubblicazione su rivista::01a Articolo in rivista
Autophagy hijacking in PBMC From COVID-19 patients results in lymphopenia / Barbati, Cristiana; Celia, Alessandra Ida; Colasanti, Tania; Vomero, Marta; Speziali, Mariangela; Putro, Erisa; Buoncuore, Giorgia; Savino, Flavia; Colafrancesco, Serena; Ucci, Federica Maria; Ciancarella, Claudia; Balbinot, Eugenia; Scarpa, Susanna; Natalucci, Francesco; Pellegrino, Greta; Ceccarelli, Fulvia; Spinelli, Francesca Romana; Mastroianni, Claudio Maria; Conti, Fabrizio; Alessandri, Cristiano. - In: FRONTIERS IN IMMUNOLOGY. - ISSN 1664-3224. - 13:(2022). [10.3389/fimmu.2022.903498]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1654875
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