ArticleThe Journal of clinical investigation2021
The autoimmune signature of hyperinflammatory multisystem inflammatory syndrome in children.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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The trial behind it
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Who cites it
90 citing papers in PubMed.
- Gastrointestinal Symptoms in Kawasaki Disease and Multisystem Inflammatory Syndrome in Children.Pediatric cardiology · 2026Article
- Multisystem Inflammatory Syndrome in Children with tailored therapy and six-month outcome.Pediatric research · 2026Article
- Long-Term Evolution of Myocardial Strain and Coronary Artery Z-Scores in Multisystem Inflammatory Syndrome in ChildrenChildren (Basel, Switzerland) · 2026Review
- Intravenous immunoglobulins in the management of acute chest syndrome in two Jehovah's Witnesses with sickle cell disease.Haematologica · 2026Article
- Lingering echoes of SARS-CoV-2: mechanistic insights and management of long COVID syndrome.Inflammopharmacology · 2026Review
- Association of blood group B and of rare variants affecting immune system with multisystem inflammatory syndrome in children in an Italian cohort.Frontiers in immunology · 2026Article
- COVID-19-associated Autoimmune and Inflammatory Diseases: Molecular Mechanisms and the Role of IVIG Therapy.Clinical reviews in allergy & immunology · 2025Review
- Mass spectrometry combined with machine learning identifies novel protein signatures as demonstrated with multisystem inflammatory syndrome in children.Scientific reports · 2025Article
- Polyclonal Vβ21.3 expansion in multisystem inflammatory syndrome in children despite SARS-CoV-2 vaccination.RMD open · 2025Article
- In depth characterisation of the proteome of MIS-C and post COVID-19 infection in children reveals inflammatory pathway activation and evidence of tissue damage.Journal of translational medicine · 2025Article
- Children with Post COVID-19 Multisystem Inflammatory Syndrome Display Unique Pathophysiological Metabolic Phenotypes.Journal of proteome research · 2025Article
- A Clinical Case of Multisystem Inflammatory Syndrome After SARS-CoV-2 Infection Associated with Group A β-Hemolytic Streptococcus Coinfection and Venous Thrombosis in a Child with Congenital Thrombophilia.Current issues in molecular biology · 2025Article
- Molecular Mimicry Drives Locally Produced Autoantibodies in Subarachnoid Neurocysticercosis.Open forum infectious diseases · 2025Article
- Observational
- Sex-based immunological differences in multisystem inflammatory syndrome in children: potential role of TFrontiers in immunology · 2025Article
- MIS-C pathogenesis: immune dysregulation & viral triggers.Frontiers in immunology · 2025Review
- Proteomic Signatures of Multisystem Inflammatory Syndrome in Children (MIS-C) Associated with COVID-19: A Narrative Review.Children (Basel, Switzerland) · 2024Review
- Kawasaki Disease Diagnosis and Treatment in over 1000 Patients: A Continuum of Dysregulated Inflammatory Responses.Biomedicines · 2024Article
- The Spectrum of Postacute Sequelae of COVID-19 in Children: From MIS-C to Long COVID.Annual review of virology · 2024Review
- Article
30 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Multisystem inflammatory syndrome in children (MIS-C) manifests as a severe and uncontrolled inflammatory response with multiorgan involvement, occurring weeks after SARS-CoV-2 infection. Here, we utilized proteomics, RNA sequencing, autoantibody arrays, and B cell receptor (BCR) repertoire analysis to characterize MIS-C immunopathogenesis and identify factors contributing to severe manifestations and intensive care unit admission. Inflammation markers, humoral immune responses, neutrophil activation, and complement and coagulation pathways were highly enriched in MIS-C patient serum, with a more hyperinflammatory profile in severe than in mild MIS-C cases. We identified a strong autoimmune signature in MIS-C, with autoantibodies targeted to both ubiquitously expressed and tissue-specific antigens, suggesting autoantigen release and excessive antigenic drive may result from systemic tissue damage. We further identified a cluster of patients with enhanced neutrophil responses as well as high anti-Spike IgG and autoantibody titers. BCR sequencing of these patients identified a strong imprint of antigenic drive with substantial BCR sequence connectivity and usage of autoimmunity-associated immunoglobulin heavy chain variable region (IGHV) genes. This cluster was linked to a TRBV11-2 expanded T cell receptor (TCR) repertoire, consistent with previous studies indicating a superantigen-driven pathogenic process. Overall, we identify a combination of pathogenic pathways that culminate in MIS-C and may inform treatment.
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