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Deciphering the state of immune silence in fatal COVID-19 patients #MMPMID33674591
Bost P; De Sanctis F; Cane S; Ugel S; Donadello K; Castellucci M; Eyal D; Fiore A; Anselmi C; Barouni RM; Trovato R; Caligola S; Lamolinara A; Iezzi M; Facciotti F; Mazzariol A; Gibellini D; De Nardo P; Tacconelli E; Gottin L; Polati E; Schwikowski B; Amit I; Bronte V
Nat Commun 2021[Mar]; 12 (1): 1428 PMID33674591show ga
Since the beginning of the SARS-CoV-2 pandemic, COVID-19 appeared as a unique disease with unconventional tissue and systemic immune features. Here we show a COVID-19 immune signature associated with severity by integrating single-cell RNA-seq analysis from blood samples and broncho-alveolar lavage fluids with clinical, immunological and functional ex vivo data. This signature is characterized by lung accumulation of naive lymphoid cells associated with a systemic expansion and activation of myeloid cells. Myeloid-driven immune suppression is a hallmark of COVID-19 evolution, highlighting arginase-1 expression with immune regulatory features of monocytes. Monocyte-dependent and neutrophil-dependent immune suppression loss is associated with fatal clinical outcome in severe patients. Additionally, our analysis shows a lung CXCR6(+) effector memory T cell subset is associated with better prognosis in patients with severe COVID-19. In summary, COVID-19-induced myeloid dysregulation and lymphoid impairment establish a condition of 'immune silence' in patients with critical COVID-19.
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Nat+Commun 2021 ; 12 (1): 1428
