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. 2024 Jan 31;230(2):e305–e317. doi: 10.1093/infdis/jiae032

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© The Author(s) 2024. Published by Oxford University Press on behalf of Infectious Diseases Society of America.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 4. — Cell death signatures distinguish multisystem inflammatory syndrome in children (MIS-C) from acute coronavirus disease 2019 (COVID-19) and innate immune cells contribute significantly to elevated cell-free DNA (cfDNA) levels in MIS-C. A and B, Total cfDNA levels, and levels of cfDNA derived from innate and adaptive immune cells in MIS-C, severe acute COVID-19 (SAC), and 35 pediatric healthy controls (HCs) with pre–COVID-19 pandemic plasma samples. Significance was tested using Wilcoxon test and adjusted for multiple comparisons by controlling the false discovery rate (FDR) using Benjamini–Hochberg method, *P < .05, **P < .01, ***P < .001, ****P < .0001. We redid the analysis without outliers (identified by Grubb test), which yielded identical results. Adjusting results for age, sex, and body mass index did not alter the results (see Supplementary Table 5 for details on P values). C, All patients exhibited significantly lower levels of cfDNA derived from adaptive immune cells compared to innate immune cells, but this was most significant for MIS-C patients (P = 2.628e-13) compared to SAC (P = .0001) and HC (P = .0075). Significance was tested using Wilcoxon test, adjusted for multiple comparisons by controlling FDR using Benjamini–Hochberg method. ***P < .001, ****P < .0001. D, Spearman correlation plot of interleukin 27, emergency myelopoiesis signature on dendritic cells and monocytes, and plasma cfDNA, and principal component (PC) analysis of parameters included in the Spearman correlation.