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  • 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[MESH]

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  • suck abstract from ncbi

    646 4.52 2022