Early IFN-α signatures and persistent dysfunction are distinguishing features of NK cells in severe COVID-19, bit.ly/3teIlId, our latest team effort in #COVID19 research lead by Jacob Natterman @LabSchultze and @AschenbrennerAC out now @ImmunityCP. [1/n]
We performed a detailed characterization of natural killer cells in 205 patients from four independent cohorts using #scRNAseq, #MCFC and #CyTOF together with functional studies. [2/n]
We found elevated IFN-α plasma levels in early severe COVD-19 alongside increased NK cell expression of ISGs and genes involved in IFN-α signaling. [3/n]
NK cells exert anti-SARS-CoV-2 activity but are functionally impaired in severe COVID-19. [4/n]
Further, NK cell dysfunction may be relevant for development of fibrotic lung disease in severe COVID-19, as NK cells exhibit impaired anti-fibrotic activity. [5/n]
Our study associates prolonged IFN-α-induced NK cell response with poorer disease outcome. [6/n]
Once more an intense and fruitful collaboration with the groups of @Sander_Lab and Birgit Sawitzki within the Deutsche COVID-19 OMICs Initiative decoi.eu… [7/n]
Suppressive myeloid cells are a hallmark of severe COVID-19 bit.ly/3hbrGyN. Our latest preprint provides insights into systemic immune responses to SARS-CoV-2 infection incl. profound alterations of the myeloid compartment associated with severe COVID-19. (1/n) #COVID19
We combined two scRNA-seq techniques and sc-proteomics in PBMC and whole blood in two independent dual-center patient cohorts (n=46 + n=54 samples) to determine changes in immune cell composition and activation in mild and severe cases of COVID-19.(2/n) #scRNAseq#CyToF
Our study reports 1) time- and severity-dependent deviations of the monocyte compartment, particularly the identification of immunosuppressive monocytes at late stages in severe COVID-19, 2) the apprearance of immature and dysfunctional granulocyte subsets in severe disease.(3/n)