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. 2021 Apr 26;11:655666. doi: 10.3389/fcimb.2021.655666

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Copyright © 2021 Nakazono, Nakamaru, Ramezanpour, Kondo, Watanabe, Hatakeyama, Kimura, Honma, Wormald, Vreugde, Suzuki and Homma

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Poly(I:C) significantly increased ACE2 and TMPRSS2 possibly via the IFN and NFκB signaling pathways in HNECs. Poly(I:C) activates both the IFN and NFκB signaling pathways by binding to TLR3, resulting in the induction of ACE2 and TMPRSS2. IFN-β upregulates ACE2 expression; however, ACE2 as well as the target genes of the NFκB signaling pathway such as TNF-α and IL-6 is suppressed by fluticasone propionate, while TMPRSS2 and an interferon-stimulated gene are not. This suggested that ACE2 in HNECs is regulated not only via the IFN signaling pathway but also via the NFκB signaling pathway.