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Zhang, Zhenguang; Kean, Iain R L; Dratva, Lisa M; Clark, John A; Syrimi, Eleni; Khan, Naeem; Daubney, Esther; White, Deborah; O'Neill, Lauran; Chisholm, Catherine; Payne, Caroline; Benkenstein, Sarah; Kupiec, Klaudia; Galassini, Rachel; Wright, Victoria; Winmill, Helen; Robbins, Ceri; Brown, Katherine; Ramnarayan, Padmanabhan; Scholefield, Barnaby; Peters, Mark; Klein, Nigel; Montgomery, Hugh; Meyer, Kerstin B; Teichmann, Sarah A; Bryant, Clare; Taylor, Graham; Pathan, Nazima
Nature communications, 05/2024, Letnik: 15, Številka: 1Journal Article
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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