Cooperative molecular mimicry drives prolonged autoinflammation in multisystem inflammatory syndrome in children
This study reveals that multisystem inflammatory syndrome in children (MIS-C) is driven by a mechanism of cooperative molecular mimicry, where SARS-CoV-2-specific T cells cross-react with self-antigens involved in prostaglandin biology and insulin metabolism, leading to persistent subclinical autoinflammation even after clinical recovery.