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000162916 005__ 20240221135016.0
000162916 0247_ $$2doi$$a10.1016/j.immuni.2021.09.002
000162916 0247_ $$2pmid$$apmid:34592166
000162916 0247_ $$2pmc$$apmc:PMC8416549
000162916 0247_ $$2ISSN$$a1074-7613
000162916 0247_ $$2ISSN$$a1097-4180
000162916 0247_ $$2altmetric$$aaltmetric:112893035
000162916 037__ $$aDZNE-2021-01569
000162916 041__ $$aEnglish
000162916 082__ $$a610
000162916 1001_ $$aKrämer, Benjamin$$b0
000162916 245__ $$aEarly IFN-α signatures and persistent dysfunction are distinguishing features of NK cells in severe COVID-19.
000162916 260__ $$aNew York, NY$$bElsevier$$c2021
000162916 3367_ $$2DRIVER$$aarticle
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000162916 520__ $$aLongitudinal analyses of the innate immune system, including the earliest time points, are essential to understand the immunopathogenesis and clinical course of coronavirus disease (COVID-19). Here, we performed a detailed characterization of natural killer (NK) cells in 205 patients (403 samples; days 2 to 41 after symptom onset) from four independent cohorts using single-cell transcriptomics and proteomics together with functional studies. We found elevated interferon (IFN)-α plasma levels in early severe COVD-19 alongside increased NK cell expression of IFN-stimulated genes (ISGs) and genes involved in IFN-α signaling, while upregulation of tumor necrosis factor (TNF)-induced genes was observed in moderate diseases. NK cells exert anti-SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) activity but are functionally impaired in severe COVID-19. Further, NK cell dysfunction may be relevant for the development of fibrotic lung disease in severe COVID-19, as NK cells exhibited impaired anti-fibrotic activity. Our study indicates preferential IFN-α and TNF responses in severe and moderate COVID-19, respectively, and associates a prolonged IFN-α-induced NK cell response with poorer disease outcome.
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000162916 650_7 $$2Other$$aCOVID-19
000162916 650_7 $$2Other$$aNK cells
000162916 650_7 $$2Other$$aTNF
000162916 650_7 $$2Other$$aantiviral
000162916 650_7 $$2Other$$alung fibrosis
000162916 650_7 $$2Other$$amoderate
000162916 650_7 $$2Other$$aproteomics
000162916 650_7 $$2Other$$ascRNA-seq
000162916 650_7 $$2Other$$asevere
000162916 650_7 $$2Other$$atype 1 IFN
000162916 650_7 $$2NLM Chemicals$$aIFNA1 protein, human
000162916 650_7 $$2NLM Chemicals$$aInterferon-alpha
000162916 650_7 $$2NLM Chemicals$$aTumor Necrosis Factor-alpha
000162916 650_2 $$2MeSH$$aBase Sequence
000162916 650_2 $$2MeSH$$aCOVID-19: immunology
000162916 650_2 $$2MeSH$$aHumans
000162916 650_2 $$2MeSH$$aImmunity, Innate: immunology
000162916 650_2 $$2MeSH$$aInflammation: immunology
000162916 650_2 $$2MeSH$$aInterferon-alpha: blood
000162916 650_2 $$2MeSH$$aInterferon-alpha: immunology
000162916 650_2 $$2MeSH$$aKiller Cells, Natural: immunology
000162916 650_2 $$2MeSH$$aPulmonary Fibrosis: pathology
000162916 650_2 $$2MeSH$$aRNA-Seq
000162916 650_2 $$2MeSH$$aSARS-CoV-2: immunology
000162916 650_2 $$2MeSH$$aSeverity of Illness Index
000162916 650_2 $$2MeSH$$aTranscriptome: genetics
000162916 650_2 $$2MeSH$$aTumor Necrosis Factor-alpha: metabolism
000162916 650_2 $$2MeSH$$aUnited Kingdom
000162916 650_2 $$2MeSH$$aUnited States
000162916 7001_ $$0P:(DE-2719)9000620$$aKnoll, Rainer$$b1$$udzne
000162916 7001_ $$0P:(DE-2719)9001512$$aBonaguro, Lorenzo$$b2$$udzne
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000162916 7001_ $$aSu, Yapeng$$b23
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000162916 7001_ $$aYuan, Dan$$b25
000162916 7001_ $$aChen, Daniel$$b26
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000162916 7001_ $$aHrusovsky, Kevin$$b31
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