Journal
NATURE IMMUNOLOGY
Volume 22, Issue 1, Pages 67-73Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41590-020-00828-7
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Funding
- Stanford University
- Chan Zuckerberg Biohub
- Searle Scholars Program
- Fast Grants
- CEND COVID Catalyst Fund
- National Institute of Allergy and Infectious Diseases of the National Institutes of Health [U19AI111825, U54CA260517, R01AI139119, R01AI130398, R01AI127877]
- Rockefeller University Center for Clinical and Translational Science [UL1 TR001866]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [ZIAAI001268, ZIAAI001271] Funding Source: NIH RePORTER
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COVID-19 is often characterized by a hyperinflammatory syndrome, and disease severity is associated with specific antibody structures that enhance inflammatory responses.
COVID-19 is often characterized by a hyperinflammatory syndrome. Wang and colleagues show that low levels of IgG fucosylation enhance interactions with activating Fc gamma receptors, boosting the inflammatory cytokines associated with severe COVID-19. Severe acute respiratory syndrome coronavirus 2 infections can cause coronavirus disease 2019 (COVID-19), which manifests with a range of severities from mild illness to life-threatening pneumonia and multi-organ failure. Severe COVID-19 is characterized by an inflammatory signature, including high levels of inflammatory cytokines, alveolar inflammatory infiltrates and vascular microthrombi. Here we show that patients with severe COVID-19 produced a unique serologic signature, including an increased likelihood of IgG1 with afucosylated Fc glycans. This Fc modification on severe acute respiratory syndrome coronavirus 2 IgGs enhanced interactions with the activating Fc gamma receptor Fc gamma RIIIa; when incorporated into immune complexes, Fc afucosylation enhanced production of inflammatory cytokines by monocytes, including interleukin-6 and tumor necrosis factor. These results show that disease severity in COVID-19 correlates with the presence of proinflammatory IgG Fc structures, including afucosylated IgG1.
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