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10.3390/cells9091975 http://scihub22266oqcxt.onion/10.3390/cells9091975 32859121!7563485!32859121     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cells 2020 ; 9 (9): ä Nephropedia Template TP {{tp|p=32859121|t=2020. SARS-CoV-2 Spike 1 Protein Controls Natural Killer Cell Activation via the HLA-E/NKG2A Pathway |pdf=|usr=}}{{32859121}} gab.com Text SARS-CoV-2 Spike 1 Protein Controls Natural Killer Cell Activation via the HLA-E/NKG2A Pathway JO: Cells http://www.kidney.de/pget.php?&tw=1&pmid=32859121 #FOAvip Natural killer cells are important in the control of viral infections. However, the role of NK cells during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has previously not been identified. Peripheral blood NK cells from SARS-CoV and SARS-CoV-2 naive subjects were evaluated for their activation, degranulation, and interferon-gamma expression in the presence of SARS-CoV and SARS-CoV-2 spike proteins. K562 and lung epithelial cells were transfected with spike proteins and co-cultured with NK cells. The analysis was performed by flow cytometry and immune fluorescence. SARS-CoV and SARS-CoV-2 spike proteins did not alter NK cell activation in a K562 in vitro model. On the contrary, SARS-CoV-2 spike 1 protein (SP1) intracellular expression by lung epithelial cells resulted in NK cell-reduced degranulation. Further experiments revealed a concomitant induction of HLA-E expression on the surface of lung epithelial cells and the recognition of an SP1-derived HLA-E-binding peptide. Simultaneously, there was increased modulation of the inhibitory receptor NKG2A/CD94 on NK cells when SP1 was expressed in lung epithelial cells. We ruled out the GATA3 transcription factor as being responsible for HLA-E increased levels and HLA-E/NKG2A interaction as implicated in NK cell exhaustion. We show for the first time that NK cells are affected by SP1 expression in lung epithelial cells via HLA-E/NKG2A interaction. The resulting NK cells' exhaustion might contribute to immunopathogenesis in SARS-CoV-2 infection. Twit Text FOAVip SARS-CoV-2 Spike 1 Protein Controls Natural Killer Cell Activation via the HLA-E/NKG2A Pathway ????Cells http://www.kidney.de/pget.php?&tw=1&pmid=32859121 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32859121 #FOAvip English Wikipedia <ref>{{Cite pmid|32859121}}</ref> SARS-CoV-2 Spike 1 Protein Controls Natural Killer Cell Activation via the HLA-E/NKG2A Pathway #MMPMID32859121 Bortolotti D; Gentili V; Rizzo S; Rotola A; Rizzo R Cells 2020[Aug]; 9 (9): ä PMID32859121show ga Natural killer cells are important in the control of viral infections. However, the role of NK cells during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has previously not been identified. Peripheral blood NK cells from SARS-CoV and SARS-CoV-2 naive subjects were evaluated for their activation, degranulation, and interferon-gamma expression in the presence of SARS-CoV and SARS-CoV-2 spike proteins. K562 and lung epithelial cells were transfected with spike proteins and co-cultured with NK cells. The analysis was performed by flow cytometry and immune fluorescence. SARS-CoV and SARS-CoV-2 spike proteins did not alter NK cell activation in a K562 in vitro model. On the contrary, SARS-CoV-2 spike 1 protein (SP1) intracellular expression by lung epithelial cells resulted in NK cell-reduced degranulation. Further experiments revealed a concomitant induction of HLA-E expression on the surface of lung epithelial cells and the recognition of an SP1-derived HLA-E-binding peptide. Simultaneously, there was increased modulation of the inhibitory receptor NKG2A/CD94 on NK cells when SP1 was expressed in lung epithelial cells. We ruled out the GATA3 transcription factor as being responsible for HLA-E increased levels and HLA-E/NKG2A interaction as implicated in NK cell exhaustion. We show for the first time that NK cells are affected by SP1 expression in lung epithelial cells via HLA-E/NKG2A interaction. The resulting NK cells' exhaustion might contribute to immunopathogenesis in SARS-CoV-2 infection. |Betacoronavirus/*chemistry[MESH] |Blood Donors[MESH] |Bronchi/cytology[MESH] |COVID-19[MESH] |Cell Degranulation/genetics[MESH] |Coculture Techniques[MESH] |Coronavirus Infections/*immunology/metabolism/virology[MESH] |Epithelial Cells/metabolism[MESH] |HLA-E Antigens[MESH] |Histocompatibility Antigens Class I/*metabolism[MESH] |Humans[MESH] |Interferon-gamma/metabolism[MESH] |K562 Cells[MESH] |Killer Cells, Natural/*immunology[MESH] |Lymphocyte Activation/*genetics[MESH] |NK Cell Lectin-Like Receptor Subfamily C/*metabolism[MESH] |Pandemics[MESH] |Pneumonia, Viral/*immunology/metabolism/virology[MESH] |RNA, Viral/genetics[MESH] |SARS-CoV-2[MESH] |Severe Acute Respiratory Syndrome/immunology/metabolism/virology[MESH] |Severe acute respiratory syndrome-related coronavirus/chemistry[MESH] |Spike Glycoprotein, Coronavirus/genetics/*metabolism[MESH]SARS-CoV-2 Spike 1 Protein Controls Natural Killer Cell Activation via(epmc).pdf DeepDyve Pubget Overpricing