[ PAPER ] · 2020 · medRxiv
The Immunology of Multisystem Inflammatory Syndrome in Children with COVID-19
C. Consiglio, N. Cotugno, F. Sardh, Christian Pou, D. Amodio, L. Rodriguez, Ziyang Tan, S. Zicari, A. Ruggiero, G. Pascucci, V. Santilli, Tessa M. Campbell, Y. Bryceson, D. Eriksson, Jun Wang, Alessandra Marchesi, T. Lakshmikanth, A. Campana, A. Villani, P. Rossi, Nils Landegren, P. Palma, P. Brodin
[ TLDR ]
The inflammatory response in MIS-C differs from the cytokine storm of severe acute COVID-19, is more similar to Kawasaki disease, but also differ from this with respect to T-cell subsets, IL-17A and biomarkers associated with arterial damage.
[ ABSTRACT ]
SARS-CoV2 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 and 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-CoV2 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, is more similar to Kawasaki disease, but also differ from this with respect to T-cell subsets, IL-17A and biomarkers associated with arterial damage. Finally, autoantibody profiling suggests endoglin, an endothelial glycoprotein as one of several candidate targets of autoantibodies in MIS-C.