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10.1038/s41586-021-04142-6 http://scihub22266oqcxt.onion/10.1038/s41586-021-04142-6 34695836!ä!34695836 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nature 2021 ; 600 (7888): 295-301 Nephropedia Template TP {{tp|p=34695836|t=2021. Untimely TGFbeta responses in COVID-19 limit antiviral functions of NK cells |pdf=|usr=}}{{34695836}} gab.com Text Untimely TGFbeta responses in COVID-19 limit antiviral functions of NK cells JO: Nature http://www.kidney.de/pget.php?&tw=1&pmid=34695836 #FOAvip SARS-CoV-2 is a single-stranded RNA virus that causes COVID-19. Given its acute and often self-limiting course, it is likely that components of the innate immune system play a central part in controlling virus replication and determining clinical outcome. Natural killer (NK) cells are innate lymphocytes with notable activity against a broad range of viruses, including RNA viruses(1,2). NK cell function may be altered during COVID-19 despite increased representation of NK cells with an activated and adaptive phenotype(3,4). Here we show that a decline in viral load in COVID-19 correlates with NK cell status and that NK cells can control SARS-CoV-2 replication by recognizing infected target cells. In severe COVID-19, NK cells show defects in virus control, cytokine production and cell-mediated cytotoxicity despite high expression of cytotoxic effector molecules. Single-cell RNA sequencing of NK cells over the time course of the COVID-19 disease spectrum reveals a distinct gene expression signature. Transcriptional networks of interferon-driven NK cell activation are superimposed by a dominant transforming growth factor-beta (TGFbeta) response signature, with reduced expression of genes related to cell-cell adhesion, granule exocytosis and cell-mediated cytotoxicity. In severe COVID-19, serum levels of TGFbeta peak during the first two weeks of infection, and serum obtained from these patients severely inhibits NK cell function in a TGFbeta-dependent manner. Our data reveal that an untimely production of TGFbeta is a hallmark of severe COVID-19 and may inhibit NK cell function and early control of the virus. Twit Text FOAVip Untimely TGFbeta responses in COVID-19 limit antiviral functions of NK cells ????Nature http://www.kidney.de/pget.php?&tw=1&pmid=34695836 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34695836 #FOAvip English Wikipedia <ref>{{Cite pmid|34695836}}</ref> Untimely TGFbeta responses in COVID-19 limit antiviral functions of NK cells #MMPMID34695836 Witkowski M; Tizian C; Ferreira-Gomes M; Niemeyer D; Jones TC; Heinrich F; Frischbutter S; Angermair S; Hohnstein T; Mattiola I; Nawrath P; McEwen S; Zocche S; Viviano E; Heinz GA; Maurer M; Kolsch U; Chua RL; Aschman T; Meisel C; Radke J; Sawitzki B; Roehmel J; Allers K; Moos V; Schneider T; Hanitsch L; Mall MA; Conrad C; Radbruch H; Duerr CU; Trapani JA; Marcenaro E; Kallinich T; Corman VM; Kurth F; Sander LE; Drosten C; Treskatsch S; Durek P; Kruglov A; Radbruch A; Mashreghi MF; Diefenbach A Nature 2021[Dec]; 600 (7888): 295-301 PMID34695836show ga SARS-CoV-2 is a single-stranded RNA virus that causes COVID-19. Given its acute and often self-limiting course, it is likely that components of the innate immune system play a central part in controlling virus replication and determining clinical outcome. Natural killer (NK) cells are innate lymphocytes with notable activity against a broad range of viruses, including RNA viruses(1,2). NK cell function may be altered during COVID-19 despite increased representation of NK cells with an activated and adaptive phenotype(3,4). Here we show that a decline in viral load in COVID-19 correlates with NK cell status and that NK cells can control SARS-CoV-2 replication by recognizing infected target cells. In severe COVID-19, NK cells show defects in virus control, cytokine production and cell-mediated cytotoxicity despite high expression of cytotoxic effector molecules. Single-cell RNA sequencing of NK cells over the time course of the COVID-19 disease spectrum reveals a distinct gene expression signature. Transcriptional networks of interferon-driven NK cell activation are superimposed by a dominant transforming growth factor-beta (TGFbeta) response signature, with reduced expression of genes related to cell-cell adhesion, granule exocytosis and cell-mediated cytotoxicity. In severe COVID-19, serum levels of TGFbeta peak during the first two weeks of infection, and serum obtained from these patients severely inhibits NK cell function in a TGFbeta-dependent manner. Our data reveal that an untimely production of TGFbeta is a hallmark of severe COVID-19 and may inhibit NK cell function and early control of the virus. |Atlases as Topic[MESH] |COVID-19/*immunology[MESH] |Gene Expression Regulation/immunology[MESH] |Humans[MESH] |Immunity, Innate[MESH] |Influenza, Human/immunology[MESH] |Killer Cells, Natural/*immunology/pathology[MESH] |RNA-Seq[MESH] |SARS-CoV-2/*immunology[MESH] |Single-Cell Analysis[MESH] |Time Factors[MESH] |Transforming Growth Factor beta/blood/*immunology[MESH] |Viral Load/immunology[MESH]Untimely TGFbeta responses in COVID-19 limit antiviral functions of NK(epmc).pdf DeepDyve Pubget Overpricing