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. 2021 Sep 9;10(9):1440. doi: 10.3390/antiox10091440

Figure 1.

Figure 1

Activation of monocyte-derived macrophages in COVID-19. Several mechanisms induce the excessive activation of monocytes/macrophages during a SARS-CoV-2 infection. The delayed production of IFN I results in the continued conscription of circulating monocytes into the pulmonary parenchyma. Activated NK and T cells also favor infiltrating cells derived from monocytes. Virus detection may trigger the activation of TLR7 as a result of the recognition of the viral single-stranded RNA. IFN I increases the expression of the SARS-CoV-2 entry receptor ACE2, allowing the virus to enter macrophages and activate cytoplasmic inflammation through NLRP3. The combination of the immune complex containing the anti-spike protein IgG with the Fcγ receptor (FcγR) on activated macrophages further promotes aberrant viral entry and causes an inflammatory cascade. CCL: CC-chemokine ligand; CXCL10: CXC-chemokine ligand 10; ISG: interferon-stimulated gene; ITAM: immune 06receptor tyrosine-based activation motif; TRAM: TRIF-related adaptor molecule; NK, natural killer. Figure generated with Biorender (https://biorender.com/ accessed on 6 September 2021).