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Arunachalam, Prabhu S; Wimmers, Florian; Mok, Chris Ka Pun; Perera, Ranawaka A P M; Scott, Madeleine; Hagan, Thomas; Sigal, Natalia; Feng, Yupeng; Bristow, Laurel; Tak-Yin Tsang, Owen; Wagh, Dhananjay; Coller, John; Pellegrini, Kathryn L; Kazmin, Dmitri; Alaaeddine, Ghina; Leung, Wai Shing; Chan, Jacky Man Chun; Chik, Thomas Shiu Hong; Choi, Chris Yau Chung; Huerta, Christopher; Paine McCullough, Michele; Lv, Huibin; Anderson, Evan; Edupuganti, Srilatha; Upadhyay, Amit A; Bosinger, Steve E; Maecker, Holden Terry; Khatri, Purvesh; Rouphael, Nadine; Peiris, Malik; Pulendran, Bali
Science, 09/2020, Letnik: 369, Številka: 6508Journal Article
Coronavirus disease 2019 (COVID-19) represents a global crisis, yet major knowledge gaps remain about human immunity to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). We analyzed immune responses in 76 COVID-19 patients and 69 healthy individuals from Hong Kong and Atlanta, Georgia, United States. In the peripheral blood mononuclear cells (PBMCs) of COVID-19 patients, we observed reduced expression of human leukocyte antigen class DR (HLA-DR) and proinflammatory cytokines by myeloid cells as well as impaired mammalian target of rapamycin (mTOR) signaling and interferon-α (IFN-α) production by plasmacytoid dendritic cells. By contrast, we detected enhanced plasma levels of inflammatory mediators-including EN-RAGE, TNFSF14, and oncostatin M-which correlated with disease severity and increased bacterial products in plasma. Single-cell transcriptomics revealed a lack of type I IFNs, reduced HLA-DR in the myeloid cells of patients with severe COVID-19, and transient expression of IFN-stimulated genes. This was consistent with bulk PBMC transcriptomics and transient, low IFN-α levels in plasma during infection. These results reveal mechanisms and potential therapeutic targets for COVID-19.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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