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10.3389/fimmu.2021.631226 http://scihub22266oqcxt.onion/10.3389/fimmu.2021.631226 33679778!7930228!33679778     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=33679778&cmd=llinks): Failed to open stream: HTTP request failed! 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Inflammation and Antiviral Immune Response Associated With Severe Progression of COVID-19 |pdf=|usr=}}{{33679778}} gab.com Text Inflammation and Antiviral Immune Response Associated With Severe Progression of COVID-19 JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=33679778 #FOAvip Coronavirus disease-2019 (COVID-19) is a novel respiratory disease induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It remains poorly understood how the host immune system responds to the infection during disease progression. We applied microarray analysis of the whole genome transcriptome to peripheral blood mononuclear cells (PBMCs) taken from severe and mild COVID-19 patients as well as healthy controls. Functional enrichment analysis of genes associated with COVID-19 severity indicated that disease progression is featured by overactivation of myeloid cells and deficient T cell function. The upregulation of TLR6 and MMP9, which promote the neutrophils-mediated inflammatory response, and the downregulation of SKAP1 and LAG3, which regulate T cells function, were associated with disease severity. Importantly, the regulation of these four genes was absent in patients with influenza A (H1N1). And compared with stimulation with hemagglutinin (HA) of H1N1 virus, the regulation pattern of these genes was unique in PBMCs response to Spike protein of SARS-CoV-2 ex vivo. Our data also suggested that severe SARS-CoV-2 infection largely silenced the response of type I interferons (IFNs) and altered the proportion of immune cells, providing a potential mechanism for the hypercytokinemia. This study indicates that SARS-CoV-2 infection impairs inflammatory and immune signatures in patients, especially those at severe stage. The potential mechanisms underpinning severe COVID-19 progression include overactive myeloid cells, impaired function of T cells, and inadequate induction of type I IFNs signaling. Twit Text FOAVip Inflammation and Antiviral Immune Response Associated With Severe Progression of COVID-19 ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=33679778 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33679778 #FOAvip English Wikipedia <ref>{{Cite pmid|33679778}}</ref> Inflammation and Antiviral Immune Response Associated With Severe Progression of COVID-19 #MMPMID33679778 Zhang Q; Meng Y; Wang K; Zhang X; Chen W; Sheng J; Qiu Y; Diao H; Li L Front Immunol 2021[]; 12 (ä): 631226 PMID33679778show ga Coronavirus disease-2019 (COVID-19) is a novel respiratory disease induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It remains poorly understood how the host immune system responds to the infection during disease progression. We applied microarray analysis of the whole genome transcriptome to peripheral blood mononuclear cells (PBMCs) taken from severe and mild COVID-19 patients as well as healthy controls. Functional enrichment analysis of genes associated with COVID-19 severity indicated that disease progression is featured by overactivation of myeloid cells and deficient T cell function. The upregulation of TLR6 and MMP9, which promote the neutrophils-mediated inflammatory response, and the downregulation of SKAP1 and LAG3, which regulate T cells function, were associated with disease severity. Importantly, the regulation of these four genes was absent in patients with influenza A (H1N1). And compared with stimulation with hemagglutinin (HA) of H1N1 virus, the regulation pattern of these genes was unique in PBMCs response to Spike protein of SARS-CoV-2 ex vivo. Our data also suggested that severe SARS-CoV-2 infection largely silenced the response of type I interferons (IFNs) and altered the proportion of immune cells, providing a potential mechanism for the hypercytokinemia. This study indicates that SARS-CoV-2 infection impairs inflammatory and immune signatures in patients, especially those at severe stage. The potential mechanisms underpinning severe COVID-19 progression include overactive myeloid cells, impaired function of T cells, and inadequate induction of type I IFNs signaling. |Adolescent[MESH] |Adult[MESH] |Aged[MESH] |Antigens, CD/immunology[MESH] |COVID-19/*immunology[MESH] |Female[MESH] |Gene Expression Profiling[MESH] |Humans[MESH] |Influenza A Virus, H1N1 Subtype/immunology[MESH] |Influenza, Human/immunology[MESH] |Interferon Type I/immunology[MESH] |Leukocytes, Mononuclear/*immunology[MESH] |Lymphocyte Activation Gene 3 Protein[MESH] |Male[MESH] |Matrix Metalloproteinase 9/immunology[MESH] |Middle Aged[MESH] |Phosphoproteins/immunology[MESH] |SARS-CoV-2/*immunology[MESH] |Signal Transduction/*immunology[MESH]Inflammation and Antiviral Immune Response Associated With Severe Prog(epmc).pdf DeepDyve Pubget Overpricing