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. 2021 Feb 26;5(5):1164–1177. doi: 10.1182/bloodadvances.2020003568

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© 2021 by The American Society of Hematology

This article is made available via the PMC Open Access Subset for unrestricted reuse and analyses in any form or by any means with acknowledgment of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global 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 6. — Model of neutrophil development and activation driving pathogenesis of severe COVID-19. We hypothesize that high levels of G-CSF drive emergency granulopoiesis, stimulating rapid neutrophil development and egress of immature neutrophils into the bloodstream. These cells then differentiate into neutrophils and are attracted to the lung, and perhaps other tissues, by the chemokine IL-8 (CXCL8). When activated, these mature neutrophils degranulate, releasing granule proteins that include resistin, lipocalin-2, HGF, and MMP-8. Neutrophil activation causes significant collateral damage that may contribute to severe COVID-19 pathology and clinical decompensation. Created with BioRender.com.