Journal article
Proinflammatory IgG Fc structures in patients with severe COVID-19
Nature immunology, Vol.22(1), pp.67-73
01/01/2021
DOI: 10.1038/s41590-020-00828-7
PMID: 33169014
Abstract
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.
Details
- Title: Subtitle
- Proinflammatory IgG Fc structures in patients with severe COVID-19
- Creators
- Saborni Chakraborty - Stanford MedicineJoseph Gonzalez - Stanford MedicineKarlie Edwards - Stanford MedicineVamsee Mallajosyula - Stanford UniversityAnthony S. Buzzanco - Stanford MedicineRobert Sherwood - Cornell UniversityCindy Buffone - Stanford MedicineNimish Kathale - Stanford MedicineSusan Providenza - Stanford MedicineMarkus M. Xie - Stanford MedicineJason R. Andrews - Stanford MedicineCatherine A. Blish - Chan Zuckerberg Biohub San FranciscoUpinder Singh - Stanford MedicineHaley Dugan - University of ChicagoPatrick C. Wilson - University of ChicagoTho D. Pham - Stanford Blood CenterScott D. Boyd - Stanford UniversityKari C. Nadeau - Stanford UniversityBenjamin A. Pinsky - Stanford MedicineSheng Zhang - Cornell UniversityMatthew J. Memoli - National Institute of Allergy and Infectious DiseasesJeffery K. Taubenberger - National Institutes of HealthTasha Morales - Kaiser Permanente Northern CaliforniaJeffrey M. Schapiro - Kaiser Permanente Northern CaliforniaGene S. Tan - University of California San DiegoPrasanna Jagannathan - Stanford MedicineTaia T. Wang - Stanford University
- Resource Type
- Journal article
- Publication Details
- Nature immunology, Vol.22(1), pp.67-73
- DOI
- 10.1038/s41590-020-00828-7
- PMID
- 33169014
- ISSN
- 1529-2908
- eISSN
- 1529-2916
- Publisher
- NATURE PORTFOLIO
- Number of pages
- 7
- Grant note
- Chan Zuckerberg Biohub; Chan Zuckerberg Initiative (CZI) U19AI111825; U54CA260517; R01AI139119; R01AI130398; R01AI127877 / National Institute of Allergy and Infectious Diseases of the National Institutes of Health; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of Allergy & Infectious Diseases (NIAID) ZIAAI001221; ZIAAI001268; ZIAAI001271; U19AI111825; R01AI139119; R01AI127877; U01AI150741; R01AI125567; P01AI097092; R01AI130398 / National Institute of Allergy and Infectious Diseases; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of Allergy & Infectious Diseases (NIAID) UL1TR001866 / National Center for Advancing Translational Sciences; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Center for Advancing Translational Sciences (NCATS) UL1 TR001866 / Rockefeller University Center for Clinical and Translational Science Fast Grants Stanford University Searle Scholars Program CEND COVID Catalyst Fund
- Language
- English
- Date published
- 01/01/2021
- Academic Unit
- Internal Medicine
- Record Identifier
- 9985244655202771
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