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10.3389/fimmu.2020.589380 http://scihub22266oqcxt.onion/10.3389/fimmu.2020.589380 33178221!7596772!33178221     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=33178221&cmd=llinks): Failed to open stream: HTTP request failed! 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T-Cell Hyperactivation and Paralysis in Severe COVID-19 Infection Revealed by Single-Cell Analysis |pdf=|usr=}}{{33178221}} gab.com Text T-Cell Hyperactivation and Paralysis in Severe COVID-19 Infection Revealed by Single-Cell Analysis JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=33178221 #FOAvip Severe COVID-19 patients show various immunological abnormalities including T-cell reduction and cytokine release syndrome, which can be fatal and is a major concern of the pandemic. However, it is poorly understood how T-cell dysregulation can contribute to the pathogenesis of severe COVID-19. Here we show single cell-level mechanisms for T-cell dysregulation in severe COVID-19, demonstrating new pathogenetic mechanisms of T-cell activation and differentiation underlying severe COVID-19. By in silico sorting CD4+ T-cells from a single cell RNA-seq dataset, we found that CD4+ T-cells were highly activated and showed unique differentiation pathways in the lung of severe COVID-19 patients. Notably, those T-cells in severe COVID-19 patients highly expressed immunoregulatory receptors and CD25, whilst repressing the expression of FOXP3. Furthermore, we show that CD25(+) hyperactivated T-cells differentiate into multiple helper T-cell lineages, showing multifaceted effector T-cells with Th1 and Th2 characteristics. Lastly, we show that CD25-expressing hyperactivated T-cells produce the protease Furin, which facilitates the viral entry of SARS-CoV-2. Collectively, CD4(+) T-cells from severe COVID-19 patients are hyperactivated and FOXP3-mediated negative feedback mechanisms are impaired in the lung, which may promote immunopathology. Therefore, our study proposes a new model of T-cell hyperactivation and paralysis that drives immunopathology in severe COVID-19. Twit Text FOAVip T-Cell Hyperactivation and Paralysis in Severe COVID-19 Infection Revealed by Single-Cell Analysis ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=33178221 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33178221 #FOAvip English Wikipedia <ref>{{Cite pmid|33178221}}</ref> T-Cell Hyperactivation and Paralysis in Severe COVID-19 Infection Revealed by Single-Cell Analysis #MMPMID33178221 Kalfaoglu B; Almeida-Santos J; Tye CA; Satou Y; Ono M Front Immunol 2020[]; 11 (ä): 589380 PMID33178221show ga Severe COVID-19 patients show various immunological abnormalities including T-cell reduction and cytokine release syndrome, which can be fatal and is a major concern of the pandemic. However, it is poorly understood how T-cell dysregulation can contribute to the pathogenesis of severe COVID-19. Here we show single cell-level mechanisms for T-cell dysregulation in severe COVID-19, demonstrating new pathogenetic mechanisms of T-cell activation and differentiation underlying severe COVID-19. By in silico sorting CD4+ T-cells from a single cell RNA-seq dataset, we found that CD4+ T-cells were highly activated and showed unique differentiation pathways in the lung of severe COVID-19 patients. Notably, those T-cells in severe COVID-19 patients highly expressed immunoregulatory receptors and CD25, whilst repressing the expression of FOXP3. Furthermore, we show that CD25(+) hyperactivated T-cells differentiate into multiple helper T-cell lineages, showing multifaceted effector T-cells with Th1 and Th2 characteristics. Lastly, we show that CD25-expressing hyperactivated T-cells produce the protease Furin, which facilitates the viral entry of SARS-CoV-2. Collectively, CD4(+) T-cells from severe COVID-19 patients are hyperactivated and FOXP3-mediated negative feedback mechanisms are impaired in the lung, which may promote immunopathology. Therefore, our study proposes a new model of T-cell hyperactivation and paralysis that drives immunopathology in severe COVID-19. |*Severity of Illness Index[MESH] |COVID-19/*immunology/virology[MESH] |Databases, Genetic[MESH] |Forkhead Transcription Factors/metabolism[MESH] |Furin/metabolism[MESH] |Humans[MESH] |Interleukin-2 Receptor alpha Subunit/metabolism[MESH] |Lymphocyte Activation/*immunology[MESH] |Paralysis/*immunology[MESH] |RNA-Seq[MESH] |Receptors, Antigen, T-Cell/metabolism[MESH] |SARS-CoV-2/*immunology[MESH] |Single-Cell Analysis/*methods[MESH] |T-Lymphocytes, Regulatory/*immunology[MESH] |Transcriptome[MESH]T-Cell Hyperactivation and Paralysis in Severe COVID-19 Infection Reve(epmc).pdf DeepDyve Pubget Overpricing