Summary
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is typically very mild and often asymptomatic in children. A complication is the rare multisystem inflammatory syndrome in children (MIS-C) associated with COVID-19, presenting 4–6 weeks after infection as high fever, organ dysfunction, and strongly elevated markers of inflammation. The pathogenesis is unclear but has overlapping features with Kawasaki disease suggestive of vasculitis and a likely autoimmune etiology. We apply systems-level analyses of blood immune cells, cytokines, and autoantibodies in healthy children, children with Kawasaki disease enrolled prior to COVID-19, children infected with SARS-CoV-2, and children presenting with MIS-C. We find that the inflammatory response in MIS-C differs from the cytokine storm of severe acute COVID-19, shares several features with Kawasaki disease, but also differs from this condition with respect to T cell subsets, interleukin (IL)-17A, and biomarkers associated with arterial damage. Finally, autoantibody profiling suggests multiple autoantibodies that could be involved in the pathogenesis of MIS-C.
【저자키워드】 COVID-19, SARS-CoV-2, IL-17A, multisystem inflammatory syndrome in children, MIS-C, autoantibodies, Kawasaki disease, systems immunology, hyperinflammation in children, 【초록키워드】 Inflammation, coronavirus, Biomarker, Cytokines, Pathogenesis, children, Infection, T cell, Asymptomatic, Fever, organ dysfunction, Mild, Vasculitis, marker, Inflammatory response, Inflammatory, autoantibody, overlapping, acute respiratory syndrome, syndrome, acute COVID-19, healthy children, feature, blood immune cells, autoimmune etiology, enrolled, involved, elevated, analysis, presenting, infected with SARS-CoV-2, the cytokine storm, with COVID-19, 【제목키워드】 with COVID-19,