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. 2017 Nov 8;61(2):381–388. doi: 10.1007/s00125-017-4460-7

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© The Author(s) 2017

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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Fig. 2 — (a) Genes in peaking clusters mapping to the interferon signalling pathway based on the IPA tool. Red, genes present in at least four peaking clusters of the strongly enterovirus-positive children; pink, genes present in at least one peaking cluster. (b–h) Child-specific expression profiles of two genes of the interferon signalling pathway, MX1 (grey) and STAT2 (black). IFNγ is also known as IFNG; IFNα/β is also known as IFNA1/B1; TC-PTP is also known as PTPN2; NF-κB p65 is also known as RELA; BCL-2 is also known as BCL2; BAK is also known as BAK1; DRIP150 is also known as MED14; G1P2 is also known as ISG15; G1P3 is also known as IFI6. EV+, enterovirus-positive; GAS, IFNG-activated sequence; ISRE, interferon-stimulated regulatory element. The five children with strongly enterovirus-positive blood samples are denoted as Strong 1–Strong 5 (b–f). The two children with weakly enterovirus-positive blood samples are denoted as Weak 1 and Weak 2 (g, h)