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Proinflammatory IgG Fc structures in patients with severe COVID-19.
Chakraborty, Saborni; Gonzalez, Joseph; Edwards, Karlie; Mallajosyula, Vamsee; Buzzanco, Anthony S; Sherwood, Robert; Buffone, Cindy; Kathale, Nimish; Providenza, Susan; Xie, Markus M; Andrews, Jason R; Blish, Catherine A; Singh, Upinder; Dugan, Haley; Wilson, Patrick C; Pham, Tho D; Boyd, Scott D; Nadeau, Kari C; Pinsky, Benjamin A; Zhang, Sheng; Memoli, Matthew J; Taubenberger, Jeffery K; Morales, Tasha; Schapiro, Jeffrey M; Tan, Gene S; Jagannathan, Prasanna; Wang, Taia T.
  • Chakraborty S; Department of Medicine, Division of Infectious Diseases, Stanford University, Stanford, CA, USA.
  • Gonzalez J; Department of Medicine, Division of Infectious Diseases, Stanford University, Stanford, CA, USA.
  • Edwards K; Department of Medicine, Division of Infectious Diseases, Stanford University, Stanford, CA, USA.
  • Mallajosyula V; Institute for Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, USA.
  • Buzzanco AS; Department of Medicine, Division of Infectious Diseases, Stanford University, Stanford, CA, USA.
  • Sherwood R; Proteomics Facility, Institute of Biotechnology, Cornell University, Ithaca, NY, USA.
  • Buffone C; Department of Medicine, Division of Infectious Diseases, Stanford University, Stanford, CA, USA.
  • Kathale N; Department of Medicine, Division of Infectious Diseases, Stanford University, Stanford, CA, USA.
  • Providenza S; Department of Medicine, Division of Infectious Diseases, Stanford University, Stanford, CA, USA.
  • Xie MM; Department of Medicine, Division of Infectious Diseases, Stanford University, Stanford, CA, USA.
  • Andrews JR; Department of Medicine, Division of Infectious Diseases, Stanford University, Stanford, CA, USA.
  • Blish CA; Department of Medicine, Division of Infectious Diseases, Stanford University, Stanford, CA, USA.
  • Singh U; Chan Zuckerberg Biohub, San Francisco, CA, USA.
  • Dugan H; Department of Medicine, Division of Infectious Diseases, Stanford University, Stanford, CA, USA.
  • Wilson PC; Department of Microbiology and Immunology, Stanford University, Stanford, CA, USA.
  • Pham TD; Department of Medicine, Section of Rheumatology, Gwen Knapp Center for Lupus and Immunology, University of Chicago, Chicago, IL, USA.
  • Boyd SD; Department of Medicine, Section of Rheumatology, Gwen Knapp Center for Lupus and Immunology, University of Chicago, Chicago, IL, USA.
  • Nadeau KC; Stanford Blood Center, Palo Alto, CA, USA.
  • Pinsky BA; Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
  • Zhang S; Sean N. Parker Center for Allergy and Asthma Research, Stanford, CA, USA.
  • Memoli MJ; Sean N. Parker Center for Allergy and Asthma Research, Stanford, CA, USA.
  • Taubenberger JK; Department of Medicine, Division of Infectious Diseases, Stanford University, Stanford, CA, USA.
  • Morales T; Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
  • Schapiro JM; Proteomics Facility, Institute of Biotechnology, Cornell University, Ithaca, NY, USA.
  • Tan GS; LID Clinical Studies Unit, Laboratory of Infectious Diseases, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
  • Jagannathan P; LID Clinical Studies Unit, Laboratory of Infectious Diseases, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
  • Wang TT; Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Nat Immunol ; 22(1): 67-73, 2021 01.
Article in English | MEDLINE | ID: covidwho-1065904
ABSTRACT
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 Fcγ receptor FcγRIIIa; 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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Full text: Available Collection: International databases Database: MEDLINE Main subject: Immunoglobulin G / Cytokines / Receptors, IgG / SARS-CoV-2 / COVID-19 Type of study: Prognostic study Limits: Adolescent / Adult / Aged / Child / Female / Humans / Male / Middle aged Language: English Journal: Nat Immunol Journal subject: Allergy and Immunology Year: 2021 Document Type: Article Affiliation country: S41590-020-00828-7

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Immunoglobulin G / Cytokines / Receptors, IgG / SARS-CoV-2 / COVID-19 Type of study: Prognostic study Limits: Adolescent / Adult / Aged / Child / Female / Humans / Male / Middle aged Language: English Journal: Nat Immunol Journal subject: Allergy and Immunology Year: 2021 Document Type: Article Affiliation country: S41590-020-00828-7