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10.15252/emmm.202114150 http://scihub22266oqcxt.onion/10.15252/emmm.202114150 34133077!8350892!34133077     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       EMBO+Mol+Med 2021 ; 13 (8): e14150 Nephropedia Template TP {{tp|p=34133077|t=2021. Long-lived macrophage reprogramming drives spike protein-mediated inflammasome activation in COVID-19 |pdf=|usr=}}{{34133077}} gab.com Text Long-lived macrophage reprogramming drives spike protein-mediated inflammasome activation in COVID-19 JO: EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=34133077 #FOAvip Innate immunity triggers responsible for viral control or hyperinflammation in COVID-19 are largely unknown. Here we show that the SARS-CoV-2 spike protein (S-protein) primes inflammasome formation and release of mature interleukin-1beta (IL-1beta) in macrophages derived from COVID-19 patients but not in macrophages from healthy SARS-CoV-2 naive individuals. Furthermore, longitudinal analyses reveal robust S-protein-driven inflammasome activation in macrophages isolated from convalescent COVID-19 patients, which correlates with distinct epigenetic and gene expression signatures suggesting innate immune memory after recovery from COVID-19. Importantly, we show that S-protein-driven IL-1beta secretion from patient-derived macrophages requires non-specific monocyte pre-activation in vivo to trigger NLRP3-inflammasome signaling. Our findings reveal that SARS-CoV-2 infection causes profound and long-lived reprogramming of macrophages resulting in augmented immunogenicity of the SARS-CoV-2 S-protein, a major vaccine antigen and potent driver of adaptive and innate immune signaling. Twit Text FOAVip Long-lived macrophage reprogramming drives spike protein-mediated inflammasome activation in COVID-19 ????EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=34133077 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34133077 #FOAvip English Wikipedia <ref>{{Cite pmid|34133077}}</ref> Long-lived macrophage reprogramming drives spike protein-mediated inflammasome activation in COVID-19 #MMPMID34133077 Theobald SJ; Simonis A; Georgomanolis T; Kreer C; Zehner M; Eisfeld HS; Albert MC; Chhen J; Motameny S; Erger F; Fischer J; Malin JJ; Grab J; Winter S; Pouikli A; David F; Boll B; Koehler P; Vanshylla K; Gruell H; Suarez I; Hallek M; Fatkenheuer G; Jung N; Cornely OA; Lehmann C; Tessarz P; Altmuller J; Nurnberg P; Kashkar H; Klein F; Koch M; Rybniker J EMBO Mol Med 2021[Aug]; 13 (8): e14150 PMID34133077show ga Innate immunity triggers responsible for viral control or hyperinflammation in COVID-19 are largely unknown. Here we show that the SARS-CoV-2 spike protein (S-protein) primes inflammasome formation and release of mature interleukin-1beta (IL-1beta) in macrophages derived from COVID-19 patients but not in macrophages from healthy SARS-CoV-2 naive individuals. Furthermore, longitudinal analyses reveal robust S-protein-driven inflammasome activation in macrophages isolated from convalescent COVID-19 patients, which correlates with distinct epigenetic and gene expression signatures suggesting innate immune memory after recovery from COVID-19. Importantly, we show that S-protein-driven IL-1beta secretion from patient-derived macrophages requires non-specific monocyte pre-activation in vivo to trigger NLRP3-inflammasome signaling. Our findings reveal that SARS-CoV-2 infection causes profound and long-lived reprogramming of macrophages resulting in augmented immunogenicity of the SARS-CoV-2 S-protein, a major vaccine antigen and potent driver of adaptive and innate immune signaling. |*COVID-19[MESH] |*Spike Glycoprotein, Coronavirus[MESH] |Humans[MESH] |Immunity, Innate[MESH] |Inflammasomes[MESH] |Interleukin-1beta[MESH] |Macrophages[MESH] |NLR Family, Pyrin Domain-Containing 3 Protein/genetics[MESH]Long-lived macrophage reprogramming drives spike protein-mediated infl(epmc).pdf DeepDyve Pubget Overpricing