Multisystem Inflammatory Syndrome in Children with COVID-19

Insights into a rare but severe complication in children with COVID-19

A study by Petter Brodin’s group at the Karolinska Institute has looked into an aspect of the COVID-19 pandemic that has perhaps not received enough attention to date. While the large majority of children infected with SARS-CoV-2 show only very mild symptoms if any, some develop high fever, organ dysfunction and express strongly elevated levels of inflammatory proteins. This condition is known as Multisystem Inflammatory Syndrome in Children (MIS-C) and exhibits several overlapping features with Kawasaki disease, an autoimmune condition in which vasculitis affects medium-sized arteries in young children.

In a study employing Olink protein analysis alongside flow cytometry and auto-antibody screening, Brodin’s team was able to show that the inflammatory response in MIS-C differs from that seen in severe acute COVID-19 in adults and shares several features with Kawasaki disease. Crucially, however, they also found important differences between MIS-C and Kawasaki, particularly with respect to the T-cell subsets involved, expression of IL-17A, and biomarkers associated with arterial damage. These findings have significant implications for the understanding and possible treatment strategies for the two diseases (e.g. targeting of IL-17A, which drives the cytokine storm in Kawasaki disease but not MIS-C). Additionally, while treatments targeting TNF-alpha and IL-6 have been suggested for severe acute COVID-19 in adults, neither of these proteins were seen to be significantly elevated in children with MIS-C

The study was recently published in Cell:

Consiglio et. al. (2020) The Immunology of Multisystem Inflammatory Syndrome in Children with COVID-19. Cell, DOI: 10.1016/j.cell.2020.09.016. – see the article here.

About the principal investigator on this study


Petter Brodin studied medicine at Karolinska Institutet and graduated in 2011 when he also defended his Ph.D. thesis in immunology at the same institution. He subsequently joined the Mark Davis laboratory at Stanford University, California. There he studied human immune system variation and the influences of heritable and non-heritable factors (Brodin et al, Cell 2015).

In 2013, he was recruited back to Sweden and the newly established Science for Life Laboratory in Solna to build up a national facility for Mass cytometry and form his own research group. Brodin and his team members have since continued to develop methods to profile human immune systems at the system level in health and disease.

He also specializes in pediatrics and has more recently focused on early human immune systems development and the influences of environmental factors. (Photograph of Petter kindly provided by Ulf Sirborn)

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