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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
Nature immunology, 01/2021, Letnik: 22, Številka: 1Journal Article
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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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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