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10.1038/s41392-020-00243-2 http://scihub22266oqcxt.onion/10.1038/s41392-020-00243-2 32712629!7381863!32712629     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       Signal+Transduct+Target+Ther 2020 ; 5 (1): 128 Nephropedia Template TP {{tp|p=32712629|t=2020. COVID-19: immunopathogenesis and Immunotherapeutics |pdf=|usr=}}{{32712629}} gab.com Text COVID-19: immunopathogenesis and Immunotherapeutics JO: Signal Transduct Target Ther http://www.kidney.de/pget.php?&tw=1&pmid=32712629 #FOAvip The recent novel coronavirus disease (COVID-19) outbreak, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is seeing a rapid increase in infected patients worldwide. The host immune response to SARS-CoV-2 appears to play a critical role in disease pathogenesis and clinical manifestations. SARS-CoV-2 not only activates antiviral immune responses, but can also cause uncontrolled inflammatory responses characterized by marked pro-inflammatory cytokine release in patients with severe COVID-19, leading to lymphopenia, lymphocyte dysfunction, and granulocyte and monocyte abnormalities. These SARS-CoV-2-induced immune abnormalities may lead to infections by microorganisms, septic shock, and severe multiple organ dysfunction. Therefore, mechanisms underlying immune abnormalities in patients with COVID-19 must be elucidated to guide clinical management of the disease. Moreover, rational management of the immune responses to SARS-CoV-2, which includes enhancing anti-viral immunity while inhibiting systemic inflammation, may be key to successful treatment. In this review, we discuss the immunopathology of COVID-19, its potential mechanisms, and clinical implications to aid the development of new therapeutic strategies against COVID-19. Twit Text FOAVip COVID-19: immunopathogenesis and Immunotherapeutics ????Signal Transduct Target Ther http://www.kidney.de/pget.php?&tw=1&pmid=32712629 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32712629 #FOAvip English Wikipedia <ref>{{Cite pmid|32712629}}</ref> COVID-19: immunopathogenesis and Immunotherapeutics #MMPMID32712629 Yang L; Liu S; Liu J; Zhang Z; Wan X; Huang B; Chen Y; Zhang Y Signal Transduct Target Ther 2020[Jul]; 5 (1): 128 PMID32712629show ga The recent novel coronavirus disease (COVID-19) outbreak, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is seeing a rapid increase in infected patients worldwide. The host immune response to SARS-CoV-2 appears to play a critical role in disease pathogenesis and clinical manifestations. SARS-CoV-2 not only activates antiviral immune responses, but can also cause uncontrolled inflammatory responses characterized by marked pro-inflammatory cytokine release in patients with severe COVID-19, leading to lymphopenia, lymphocyte dysfunction, and granulocyte and monocyte abnormalities. These SARS-CoV-2-induced immune abnormalities may lead to infections by microorganisms, septic shock, and severe multiple organ dysfunction. Therefore, mechanisms underlying immune abnormalities in patients with COVID-19 must be elucidated to guide clinical management of the disease. Moreover, rational management of the immune responses to SARS-CoV-2, which includes enhancing anti-viral immunity while inhibiting systemic inflammation, may be key to successful treatment. In this review, we discuss the immunopathology of COVID-19, its potential mechanisms, and clinical implications to aid the development of new therapeutic strategies against COVID-19. |*Betacoronavirus/immunology/pathogenicity[MESH] |*Coronavirus Infections/epidemiology/immunology/therapy[MESH] |*Disease Outbreaks[MESH] |*Immunity, Innate[MESH] |*Immunotherapy[MESH] |*Pandemics[MESH] |*Pneumonia, Viral/epidemiology/immunology/therapy[MESH] |*Shock, Septic/epidemiology/immunology/therapy[MESH] |COVID-19[MESH] |Cytokines/immunology[MESH] |Humans[MESH]COVID-19: immunopathogenesis and Immunotherapeutics (epmc).pdf DeepDyve Pubget Overpricing