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.

严重急性呼吸综合征冠状病毒 2 感染可导致 2019 冠状病毒病 (COVID-19)，其严重程度从轻微疾病到危及生命的肺炎和多器官衰竭不等。严重的 COVID-19 的特点是炎症特征，包括高水平的炎症细胞因子、肺泡炎症浸润和血管微血栓。在这里，我们展示了重症 COVID-19 患者产生了独特的血清学特征，包括 IgG1 与无岩藻糖基化 Fc 聚糖的可能性增加。对严重急性呼吸综合征冠状病毒 2 IgG 的 Fc 修饰增强了与激活 Fcγ 受体 FcγRIIIa 的相互作用；当掺入免疫复合物时，Fc 无岩藻糖基化可增强单核细胞产生炎性细胞因子，包括白细胞介素 6 和肿瘤坏死因子。这些结果表明，COVID-19 疾病的严重程度与促炎 IgG Fc 结构（包括无岩藻糖基化 IgG1）的存在相关。