ArticleNature communications2024
Enhanced CD95 and interleukin 18 signalling accompany T cell receptor Vβ21.3+ activation in multi-inflammatory syndrome in children.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Bone targeted microenvironment actuated engineered exosomes for precision therapy of IBD associated bone loss.Bioactive materials · 2026Article
- High expression of interleukin-18 receptor alpha correlates with severe respiratory viral disease and defines T cells with reduced cytotoxic signatures.Nature communications · 2025Article
- Identification of potential drug targets for achalasia from genetic insights: a Mendelian randomization study.Journal of cardiothoracic surgery · 2025Article
- Distinct type 1 immune networks underlie the severity of restrictive lung disease after COVID-19.Nature immunology · 2025Article
- SARS-CoV-2 spike does not interact with the T cell receptor or directly activate T cells.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
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Authors and funding
28 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multisystem inflammatory syndrome in children is a post-infectious presentation SARS-CoV-2 associated with expansion of the T cell receptor Vβ21.3+ T-cell subgroup. Here we apply muti-single cell omics to compare the inflammatory process in children with acute respiratory COVID-19 and those presenting with non SARS-CoV-2 infections in children. Here we show that in Multi-Inflammatory Syndrome in Children (MIS-C), the natural killer cell and monocyte population demonstrate heightened CD95 (Fas) and Interleuking 18 receptor expression. Additionally, TCR Vβ21.3+ CD4+ T-cells exhibit skewed differentiation towards T helper 1, 17 and regulatory T cells, with increased expression of the co-stimulation receptors ICOS, CD28 and interleukin 18 receptor. We observe no functional evidence for NLRP3 inflammasome pathway overactivation, though MIS-C monocytes show elevated active caspase 8. This, coupled with raised IL18 mRNA expression in CD16- NK cells on single cell RNA sequencing analysis, suggests interleukin 18 and CD95 signalling may trigger activation of TCR Vβ21.3+ T-cells in MIS-C, driven by increased IL-18 production from activated monocytes and CD16- Natural Killer cells.
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