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10.1038/s41590-021-00937-x http://scihub22266oqcxt.onion/10.1038/s41590-021-00937-x 33963333!8882317!33963333     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Immunol 2021 ; 22 (7): 829-838 Nephropedia Template TP {{tp|p=33963333|t=2021. TLR2 senses the SARS-CoV-2 envelope protein to produce inflammatory cytokines |pdf=|usr=}}{{33963333}} gab.com Text TLR2 senses the SARS-CoV-2 envelope protein to produce inflammatory cytokines JO: Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=33963333 #FOAvip The innate immune response is critical for recognizing and controlling infections through the release of cytokines and chemokines. However, severe pathology during some infections, including SARS-CoV-2, is driven by hyperactive cytokine release, or a cytokine storm. The innate sensors that activate production of proinflammatory cytokines and chemokines during COVID-19 remain poorly characterized. In the present study, we show that both TLR2 and MYD88 expression were associated with COVID-19 disease severity. Mechanistically, TLR2 and Myd88 were required for beta-coronavirus-induced inflammatory responses, and TLR2-dependent signaling induced the production of proinflammatory cytokines during coronavirus infection independent of viral entry. TLR2 sensed the SARS-CoV-2 envelope protein as its ligand. In addition, blocking TLR2 signaling in vivo provided protection against the pathogenesis of SARS-CoV-2 infection. Overall, our study provides a critical understanding of the molecular mechanism of beta-coronavirus sensing and inflammatory cytokine production, which opens new avenues for therapeutic strategies to counteract the ongoing COVID-19 pandemic. Twit Text FOAVip TLR2 senses the SARS-CoV-2 envelope protein to produce inflammatory cytokines ????Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=33963333 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33963333 #FOAvip English Wikipedia <ref>{{Cite pmid|33963333}}</ref> TLR2 senses the SARS-CoV-2 envelope protein to produce inflammatory cytokines #MMPMID33963333 Zheng M; Karki R; Williams EP; Yang D; Fitzpatrick E; Vogel P; Jonsson CB; Kanneganti TD Nat Immunol 2021[Jul]; 22 (7): 829-838 PMID33963333show ga The innate immune response is critical for recognizing and controlling infections through the release of cytokines and chemokines. However, severe pathology during some infections, including SARS-CoV-2, is driven by hyperactive cytokine release, or a cytokine storm. The innate sensors that activate production of proinflammatory cytokines and chemokines during COVID-19 remain poorly characterized. In the present study, we show that both TLR2 and MYD88 expression were associated with COVID-19 disease severity. Mechanistically, TLR2 and Myd88 were required for beta-coronavirus-induced inflammatory responses, and TLR2-dependent signaling induced the production of proinflammatory cytokines during coronavirus infection independent of viral entry. TLR2 sensed the SARS-CoV-2 envelope protein as its ligand. In addition, blocking TLR2 signaling in vivo provided protection against the pathogenesis of SARS-CoV-2 infection. Overall, our study provides a critical understanding of the molecular mechanism of beta-coronavirus sensing and inflammatory cytokine production, which opens new avenues for therapeutic strategies to counteract the ongoing COVID-19 pandemic. |Animals[MESH] |COVID-19 Drug Treatment[MESH] |COVID-19/complications/diagnosis/*immunology/virology[MESH] |Chlorocebus aethiops[MESH] |Coronavirus Envelope Proteins/*metabolism[MESH] |Cytokine Release Syndrome/diagnosis/*immunology[MESH] |Cytokines/metabolism[MESH] |Disease Models, Animal[MESH] |Female[MESH] |Gene Expression Profiling[MESH] |Humans[MESH] |Immunity, Innate/drug effects[MESH] |Leukocytes, Mononuclear[MESH] |Macrophages[MESH] |Male[MESH] |Mice[MESH] |Mice, Knockout[MESH] |Myeloid Differentiation Factor 88/genetics/metabolism[MESH] |Primary Cell Culture[MESH] |SARS-CoV-2/*immunology/metabolism/pathogenicity[MESH] |Severity of Illness Index[MESH] |Signal Transduction/drug effects/genetics/immunology[MESH] |Toll-Like Receptor 2/antagonists & inhibitors/genetics/*metabolism[MESH]TLR2 senses the SARS-CoV-2 envelope protein to produce inflammatory cy(epmc).pdf DeepDyve Pubget Overpricing