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. 2021 Feb 22:1–14. doi: 10.1080/08830185.2021.1884248

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© 2021 Taylor & Francis Group, LLC

This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

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Figure 1. — IL-6 and GM-CSF in NF-?B pathways. A. The N and S protein of SARS-CoV-2 interact with the NF-?B complex, leading to phosphorylation and degradation of I?B, and to the release of NF-?B dimers and translocation from the cytoplasm to the nucleus. The NF-?B dimers further bind to DNA binding sites and upregulate the expression of target genes such as IL-6, TNF-? and GM-CSF. B. GM-CSF further stimulates CD14 + CD16+ monocytes to produce higher levels of IL-6 and other inflammatory cytokines. C. By promoting the production of other cytokines and chemokines, differentiation of monocyte and macrophage, attraction of other immune cells and inhibiting Treg cells, IL-6 may play an important role in apoptosis of T cells and development of CRS.