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10.1016/j.it.2021.02.003 http://scihub22266oqcxt.onion/10.1016/j.it.2021.02.003 33622601!7879020!33622601     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 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Trends+Immunol 2021 ; 42 (4): 312-322 Nephropedia Template TP {{tp|p=33622601|t=2021. Dual Nature of Type I Interferons in SARS-CoV-2-Induced Inflammation |pdf=|usr=}}{{33622601}} gab.com Text Dual Nature of Type I Interferons in SARS-CoV-2-Induced Inflammation JO: Trends Immunol http://www.kidney.de/pget.php?&tw=1&pmid=33622601 #FOAvip Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The ability of our cells to secrete type I interferons (IFN-Is) is essential for the control of virus replication and for effective antiviral immune responses; for this reason, viruses have evolved the means to antagonize IFN-I. Inhibition of IFN-I production is pronounced in SARS-CoV-2 infection, which can impair the adaptive immune response and exacerbate inflammatory disease at late stages of infection. However, therapeutic boosting of IFN-I offers a narrow time window for efficacy and safety. Here, we discuss how limits placed on IFN-I by SARS-CoV-2 shape the immune response and whether this might be countered with therapeutic approaches and vaccine design. Twit Text FOAVip Dual Nature of Type I Interferons in SARS-CoV-2-Induced Inflammation ????Trends Immunol http://www.kidney.de/pget.php?&tw=1&pmid=33622601 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33622601 #FOAvip English Wikipedia <ref>{{Cite pmid|33622601}}</ref> Dual Nature of Type I Interferons in SARS-CoV-2-Induced Inflammation #MMPMID33622601 King C; Sprent J Trends Immunol 2021[Apr]; 42 (4): 312-322 PMID33622601show ga Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The ability of our cells to secrete type I interferons (IFN-Is) is essential for the control of virus replication and for effective antiviral immune responses; for this reason, viruses have evolved the means to antagonize IFN-I. Inhibition of IFN-I production is pronounced in SARS-CoV-2 infection, which can impair the adaptive immune response and exacerbate inflammatory disease at late stages of infection. However, therapeutic boosting of IFN-I offers a narrow time window for efficacy and safety. Here, we discuss how limits placed on IFN-I by SARS-CoV-2 shape the immune response and whether this might be countered with therapeutic approaches and vaccine design. |COVID-19/complications/*immunology[MESH] |Humans[MESH] |Inflammation/*immunology/virology[MESH] |Interferon Type I/*immunology[MESH]Dual Nature of Type I Interferons in SARS-CoV-2-Induced Inflammation (epmc).pdf DeepDyve Pubget Overpricing