ArticleThe Journal of experimental medicine2022
TIM3+ TRBV11-2 T cells and IFNγ signature in patrolling monocytes and CD16+ NK cells delineate MIS-C.
Article in The Journal of experimental medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.
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Who cites it
61 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.
- Clinical presentation, diagnosis and management of multisystem inflammatory syndrome in children (MIS-C): a systematic review.BMJ paediatrics open · 2024Pooled it
- Superantigens as Contributors to the Etiology of Kawasaki Disease Shock Syndrome.Journal of clinical medicine · 2026Article
- Decoding Undesirable Inflammatory Responses of Nucleic Acid-Delivering Lipid Nanoparticles.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Engineered APP C-terminus Alters Its Native Transcript Dynamics in Differentiated SH-SY5Y-Derived Neurons.Molecular neurobiology · 2026Article
- Shared TCR Vβ21.3+ T cell immunological signature between MIS-A and MIS-C.Journal of human immunity · 2026Article
- Ozone exposure is positively correlated with the occurrence of Kawasaki disease in Chinese children.Pediatric research · 2026Article
- C/EBPβ-induced alternative splicing of RCAN1 generates a potent TCR-T target in mesenchymal glioblastoma.Cellular & molecular immunology · 2026Article
- The seven enigmas of SARS-CoV-2: from the past to the future.Journal of human immunity · 2025Article
- Article
- 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
- Review
- Observational
- Distinctive T-cell receptor repertoire in paediatric inflammatory multisystem syndrome temporally associated with coronavirus disease 2019/multisystem inflammatory syndrome in children patients: possible thymus involvement.Clinical and experimental immunology · 2025Article
- Heterozygous BTNL8 variants in individuals with multisystem inflammatory syndrome in children (MIS-C).The Journal of experimental medicine · 2024Article
- T cell receptor-centric perspective to multimodal single-cell data analysis.Science advances · 2024Article
- Inborn Error of WAS Presenting with SARS-CoV-2-Related Multisystem Inflammatory Syndrome in Children.Journal of clinical immunology · 2024Article
- NK Cell and Monocyte Dysfunction in Multisystem Inflammatory Syndrome in Children.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- The Microbe, the Infection Enigma, and the Host.Annual review of microbiology · 2024Review
- The Spectrum of Postacute Sequelae of COVID-19 in Children: From MIS-C to Long COVID.Annual review of virology · 2024Review
- The complex landscape of immune dysregulation in multisystem inflammatory syndrome in children with COVID-19.Life medicine · 2024Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
42 authors at 6 institutions in 4 countries.
Funding
Abstract
In rare instances, pediatric SARS-CoV-2 infection results in a novel immunodysregulation syndrome termed multisystem inflammatory syndrome in children (MIS-C). We compared MIS-C immunopathology with severe COVID-19 in adults. MIS-C does not result in pneumocyte damage but is associated with vascular endotheliitis and gastrointestinal epithelial injury. In MIS-C, the cytokine release syndrome is characterized by IFNγ and not type I interferon. Persistence of patrolling monocytes differentiates MIS-C from severe COVID-19, which is dominated by HLA-DRlo classical monocytes. IFNγ levels correlate with granzyme B production in CD16+ NK cells and TIM3 expression on CD38+/HLA-DR+ T cells. Single-cell TCR profiling reveals a skewed TCRβ repertoire enriched for TRBV11-2 and a superantigenic signature in TIM3+/CD38+/HLA-DR+ T cells. Using NicheNet, we confirm IFNγ as a central cytokine in the communication between TIM3+/CD38+/HLA-DR+ T cells, CD16+ NK cells, and patrolling monocytes. Normalization of IFNγ, loss of TIM3, quiescence of CD16+ NK cells, and contraction of patrolling monocytes upon clinical resolution highlight their potential role in MIS-C immunopathogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.