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10.1002/eji.202149656 http://scihub22266oqcxt.onion/10.1002/eji.202149656 35099061!9015339!35099061     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=35099061&cmd=llinks): Failed to open stream: HTTP request failed! 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SARS-CoV-2 infection activates dendritic cells via cytosolic receptors rather than extracellular TLRs |pdf=|usr=}}{{35099061}} gab.com Text SARS-CoV-2 infection activates dendritic cells via cytosolic receptors rather than extracellular TLRs JO: Eur J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=35099061 #FOAvip Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19), an infectious disease characterized by strong induction of inflammatory cytokines, progressive lung inflammation, and potentially multiorgan dysfunction. It remains unclear how SARS-CoV-2 infection leads to immune activation. The Spike (S) protein of SARS-CoV-2 has been suggested to trigger TLR4 and thereby activate immunity. Here, we have investigated the role of TLR4 in SARS-CoV-2 infection and immunity. Neither exposure of isolated S protein, SARS-CoV-2 pseudovirus nor primary SARS-CoV-2 isolate induced TLR4 activation in a TLR4-expressing cell line. Human monocyte-derived DCs express TLR4 but not angiotensin converting enzyme 2 (ACE2), and DCs were not infected by SARS-CoV-2. Notably, neither S protein nor SARS-CoV-2 induced DC maturation or cytokines, indicating that both S protein and SARS-CoV-2 virus particles do not trigger extracellular TLRs including TLR4. Ectopic expression of ACE2 in DCs led to efficient infection by SARS-CoV-2 and, strikingly, efficient type I IFN and cytokine responses. These data strongly suggest that not extracellular TLRs but intracellular viral sensors are key players in sensing SARS-CoV-2. These data imply that SARS-CoV-2 escapes direct sensing by TLRs, which might underlie the lack of efficient immunity to SARS-CoV-2 early during infection. Twit Text FOAVip SARS-CoV-2 infection activates dendritic cells via cytosolic receptors rather than extracellular TLRs ????Eur J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=35099061 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35099061 #FOAvip English Wikipedia <ref>{{Cite pmid|35099061}}</ref> SARS-CoV-2 infection activates dendritic cells via cytosolic receptors rather than extracellular TLRs #MMPMID35099061 van der Donk LEH; Eder J; van Hamme JL; Brouwer PJM; Brinkkemper M; van Nuenen AC; van Gils MJ; Sanders RW; Kootstra NA; Bermejo-Jambrina M; Geijtenbeek TBH Eur J Immunol 2022[Apr]; 52 (4): 646-655 PMID35099061show ga Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19), an infectious disease characterized by strong induction of inflammatory cytokines, progressive lung inflammation, and potentially multiorgan dysfunction. It remains unclear how SARS-CoV-2 infection leads to immune activation. The Spike (S) protein of SARS-CoV-2 has been suggested to trigger TLR4 and thereby activate immunity. Here, we have investigated the role of TLR4 in SARS-CoV-2 infection and immunity. Neither exposure of isolated S protein, SARS-CoV-2 pseudovirus nor primary SARS-CoV-2 isolate induced TLR4 activation in a TLR4-expressing cell line. Human monocyte-derived DCs express TLR4 but not angiotensin converting enzyme 2 (ACE2), and DCs were not infected by SARS-CoV-2. Notably, neither S protein nor SARS-CoV-2 induced DC maturation or cytokines, indicating that both S protein and SARS-CoV-2 virus particles do not trigger extracellular TLRs including TLR4. Ectopic expression of ACE2 in DCs led to efficient infection by SARS-CoV-2 and, strikingly, efficient type I IFN and cytokine responses. These data strongly suggest that not extracellular TLRs but intracellular viral sensors are key players in sensing SARS-CoV-2. These data imply that SARS-CoV-2 escapes direct sensing by TLRs, which might underlie the lack of efficient immunity to SARS-CoV-2 early during infection. |*COVID-19/immunology[MESH] |*Dendritic Cells/immunology[MESH] |*Spike Glycoprotein, Coronavirus/immunology[MESH] |*Toll-Like Receptor 4/immunology[MESH] |Cell Line[MESH] |Humans[MESH]SARS-CoV-2 infection activates dendritic cells via cytosolic receptors(epmc).pdf DeepDyve Pubget Overpricing