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10.3389/fimmu.2021.741502 http://scihub22266oqcxt.onion/10.3389/fimmu.2021.741502 34671355!8521106!34671355     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\34671355.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Front+Immunol 2021 ; 12 (ä): 741502 Nephropedia Template TP {{tp|p=34671355|t=2021. Defining the Innate Immune Responses for SARS-CoV-2-Human Macrophage Interactions |pdf=|usr=}}{{34671355}} gab.com Text Defining the Innate Immune Responses for SARS-CoV-2-Human Macrophage Interactions JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34671355 #FOAvip Host innate immune response follows severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, and it is the driver of the acute respiratory distress syndrome (ARDS) amongst other inflammatory end-organ morbidities. Such life-threatening coronavirus disease 2019 (COVID-19) is heralded by virus-induced activation of mononuclear phagocytes (MPs; monocytes, macrophages, and dendritic cells). MPs play substantial roles in aberrant immune secretory activities affecting profound systemic inflammation and end-organ malfunctions. All follow the presence of persistent viral components and virions without evidence of viral replication. To elucidate SARS-CoV-2-MP interactions we investigated transcriptomic and proteomic profiles of human monocyte-derived macrophages. While expression of the SARS-CoV-2 receptor, the angiotensin-converting enzyme 2, paralleled monocyte-macrophage differentiation, it failed to affect productive viral infection. In contrast, simple macrophage viral exposure led to robust pro-inflammatory cytokine and chemokine expression but attenuated type I interferon (IFN) activity. Both paralleled dysregulation of innate immune signaling pathways, specifically those linked to IFN. We conclude that the SARS-CoV-2-infected host mounts a robust innate immune response characterized by a pro-inflammatory storm heralding end-organ tissue damage. Twit Text FOAVip Defining the Innate Immune Responses for SARS-CoV-2-Human Macrophage Interactions ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34671355 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34671355 #FOAvip English Wikipedia <ref>{{Cite pmid|34671355}}</ref> Defining the Innate Immune Responses for SARS-CoV-2-Human Macrophage Interactions #MMPMID34671355 Abdelmoaty MM; Yeapuri P; Machhi J; Olson KE; Shahjin F; Kumar V; Zhou Y; Liang J; Pandey K; Acharya A; Byrareddy SN; Mosley RL; Gendelman HE Front Immunol 2021[]; 12 (ä): 741502 PMID34671355show ga Host innate immune response follows severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, and it is the driver of the acute respiratory distress syndrome (ARDS) amongst other inflammatory end-organ morbidities. Such life-threatening coronavirus disease 2019 (COVID-19) is heralded by virus-induced activation of mononuclear phagocytes (MPs; monocytes, macrophages, and dendritic cells). MPs play substantial roles in aberrant immune secretory activities affecting profound systemic inflammation and end-organ malfunctions. All follow the presence of persistent viral components and virions without evidence of viral replication. To elucidate SARS-CoV-2-MP interactions we investigated transcriptomic and proteomic profiles of human monocyte-derived macrophages. While expression of the SARS-CoV-2 receptor, the angiotensin-converting enzyme 2, paralleled monocyte-macrophage differentiation, it failed to affect productive viral infection. In contrast, simple macrophage viral exposure led to robust pro-inflammatory cytokine and chemokine expression but attenuated type I interferon (IFN) activity. Both paralleled dysregulation of innate immune signaling pathways, specifically those linked to IFN. We conclude that the SARS-CoV-2-infected host mounts a robust innate immune response characterized by a pro-inflammatory storm heralding end-organ tissue damage. |*Immunity, Innate/genetics[MESH] |Angiotensin-Converting Enzyme 2/genetics/metabolism[MESH] |COVID-19/immunology/metabolism/*virology[MESH] |Cells, Cultured[MESH] |Cytokines/genetics/metabolism[MESH] |Gene Expression Profiling[MESH] |Gene Regulatory Networks[MESH] |Host-Pathogen Interactions[MESH] |Humans[MESH] |Inflammation Mediators/metabolism[MESH] |Macrophages/immunology/metabolism/*virology[MESH] |Proteome[MESH] |Proteomics[MESH] |Receptors, Virus/genetics/metabolism[MESH] |SARS-CoV-2/immunology/*pathogenicity[MESH] |Signal Transduction[MESH]Defining the Innate Immune Responses for SARS-CoV-2-Human Macrophage (epmc).pdf DeepDyve Pubget Overpricing