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Nat Immunol . TLR2 senses the SARS-CoV-2 envelope protein to produce inflammatory cytokines

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  • Nat Immunol . TLR2 senses the SARS-CoV-2 envelope protein to produce inflammatory cytokines


    Nat Immunol


    . 2021 May 7.
    doi: 10.1038/s41590-021-00937-x. Online ahead of print.
    TLR2 senses the SARS-CoV-2 envelope protein to produce inflammatory cytokines


    Min Zheng 1 , Rajendra Karki 1 , Evan Peter Williams 2 , Dong Yang 3 , Elizabeth Fitzpatrick 3 , Peter Vogel 4 , Colleen Beth Jonsson 2 , Thirumala-Devi Kanneganti 5



    Affiliations

    Abstract

    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 ?-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 ?-coronavirus sensing and inflammatory cytokine production, which opens new avenues for therapeutic strategies to counteract the ongoing COVID-19 pandemic.


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