Cell
. 2020 Sep 6;S0092-8674(20)31157-0.
doi: 10.1016/j.cell.2020.09.016. Online ahead of print.
The Immunology of Multisystem Inflammatory Syndrome in Children with COVID-19
Camila Rosat Consiglio 1 , Nicola Cotugno 2 , Fabian Sardh 3 , Christian Pou 1 , Donato Amodio 2 , Lucie Rodriguez 1 , Ziyang Tan 1 , Sonia Zicari 4 , Alessandra Ruggiero 4 , Giuseppe Rubens Pascucci 4 , Veronica Santilli 5 , Tessa Campbell 6 , Yenan Bryceson 6 , Daniel Eriksson 7 , Jun Wang 1 , Alessandra Marchesi 8 , Tadepally Lakshmikanth 1 , Andrea Campana 8 , Alberto Villani 8 , Paolo Rossi 9 , CACTUS Study Team; Nils Landegren 10 , Paolo Palma 11 , Petter Brodin 12
Affiliations
- PMID: 32966765
- DOI: 10.1016/j.cell.2020.09.016
Abstract
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.
Keywords: COVID-19; IL-17A; Kawasaki disease; MIS-C; SARS-CoV-2; autoantibodies; hyperinflammation in children; multisystem inflammatory syndrome in children; systems immunology.
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