The DOI matches its Crossref record; 25 of the 25 references it cites were found in a registry or an index.
FcγR-mediated SARS-CoV-2 infection of monocytes activates inflammation
Open accessAbstract
SARS-CoV-2 can cause acute respiratory distress and death in some patients1. Although severe COVID-19 is linked to substantial inflammation, how SARS-CoV-2 triggers inflammation is not clear2. Monocytes and macrophages are sentinel cells that sense invasive infection to form inflammasomes that activate caspase-1 and gasdermin D, leading to inflammatory death (pyroptosis) and the release of potent inflammatory mediators3. Here we show that about 6% of blood monocytes of patients with COVID-19 are infected with SARS-CoV-2. Monocyte infection depends on the uptake of antibody-opsonized virus by Fcγ receptors. The plasma of vaccine recipients does not promote antibody-dependent monocyte infection. SARS-CoV-2 begins to replicate in monocytes, but infection is aborted, and infectious virus is not detected in the supernatants of cultures of infected monocytes. Instead, infected cells undergo pyroptosis mediated by activation of NLRP3 and AIM2 inflammasomes, caspase-1 and gasdermin D. Moreover, tissue-resident macrophages, but not infected epithelial and endothelial cells, from lung autopsies from patients with COVID-19 have activated inflammasomes. Taken together, these findings suggest that antibody-mediated SARS-CoV-2 uptake by monocytes and macrophages triggers inflammatory cell death that aborts the production of infectious virus but causes systemic inflammation that contributes to COVID-19 pathogenesis. Antibody-mediated SARS-CoV-2 uptake by monocytes and macrophages triggers inflammatory cell death that aborts the production of infectious virus but causes systemic inflammation that contributes to COVID-19 pathogenesis.
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Cites
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Inflammasome-activated gasdermin D causes pyroptosis by forming membrane pores
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Self-citationImpaired type I interferon activity and inflammatory responses in severe COVID-19 patients
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An inflammatory cytokine signature predicts COVID-19 severity and survival
Del Valle, D. M., Kim-Schulze, S., Huang, H.-H., Beckmann, N. D., Nirenberg, S., Wang, B., Lavin, Y., Swartz, T. H., Madduri, D., Stock, A., et al. (2020) · Nature Medicine · doi:10.1038/s41591-020-1051-9 · Cited by 2,605
Pathological inflammation in patients with COVID-19: a key role for monocytes and macrophages
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Interleukin-1 in the pathogenesis and treatment of inflammatory diseases
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REGN-COV2, a Neutralizing Antibody Cocktail, in Outpatients with Covid-19
Weinreich, D. M., Sivapalasingam, S., Norton, T., Ali, S., Gao, H., Bhore, R., Musser, B. J., Soo, Y., Rofail, D., Im, J., et al. (2021) · New England Journal of Medicine · doi:10.1056/nejmoa2035002 · Cited by 1,642
Cited by
The NLRP3 inflammasome: contributions to inflammation-related diseases
Chen, Y., Ye, X., Escames, G., Lei, W., Zhang, X., Li, M., Jing, T., Yao, Y., Qiu, Z., Wang, Z., et al. (2023) · Cellular & Molecular Biology Letters · doi:10.1186/s11658-023-00462-9 · Cited by 492
A 360° view of the inflammasome: Mechanisms of activation, cell death, and diseases
Barnett, K. C., Li, S., Liang, K., & Ting, J. P.-Y. (2023) · Cell · doi:10.1016/j.cell.2023.04.025 · Cited by 458
COVID-19 and cellular senescence
Schmitt, C. A., Tchkonia, T., Niedernhofer, L. J., Robbins, P. D., Kirkland, J. L., & Lee, S. (2023) · Nature Reviews Immunology · doi:10.1038/s41577-022-00785-2 · Cited by 153
Baricitinib attenuates the proinflammatory phase of COVID-19 driven by lung-infiltrating monocytes
Dobosh, B., Zandi, K., Giraldo, D. M., Goh, S. L., Musall, K., Aldeco, M., LeCher, J., Giacalone, V. D., Yang, J., Eddins, D. J., et al. (2022) · Cell Reports · doi:10.1016/j.celrep.2022.110945 · Cited by 19
Tian, C., Ao, Z., Cerneckis, J., Cai, H., Chen, L., Niu, H., Takayama, K., Kim, J., Shi, Y., Gu, M., et al. (2025) · Science Advances · doi:10.1126/sciadv.adu2708 · Cited by 9
“Peripheral monocytes, a crucial component of the peripheral immune system, are gaining increasing recognition for their importance in inflammation ( 11 , 12 ), which has generated substantial interest in their role in AD neuroinflammation and potential impact on disease progression.”
Metadata
- Authors
- Junqueira, C., Crespo, Â., Ranjbar, S., de Lacerda, L. B., Lewandrowski, M., Ingber, J., Parry, B., Ravid, S., Clark, S., Schrimpf, M. R., Ho, F., Beakes, C., Margolin, J., Russell, N., Kays, K., Boucau, J., Das Adhikari, U., Vora, S. M., Leger, V., Gehrke, L., Henderson, L. A., Janssen, E., Kwon, D., Sander, C., Abraham, J., Goldberg, M. B., Wu, H., Mehta, G., Bell, S., Goldfeld, A. E., Filbin, M. R., & Lieberman, J.
- Venue
- Nature
- Published
- 2022-04-06
- Volume
- 606
- Issue
- 7914
- Pages
- 576-584
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W4225890110
- Cited by
- 631
- References
- 25
- FWCI
- 39.29
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Junqueira, C., Crespo, Â., Ranjbar, S., de Lacerda, L. B., Lewandrowski, M., Ingber, J., Parry, B., Ravid, S., Clark, S., Schrimpf, M. R., Ho, F., Beakes, C., Margolin, J., Russell, N., Kays, K., Boucau, J., Das Adhikari, U., Vora, S. M., Leger, V., . . . Lieberman, J. (2022). FcγR-mediated SARS-CoV-2 infection of monocytes activates inflammation. Nature. https://doi.org/10.1038/s41586-022-04702-4
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.