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. Author manuscript; available in PMC: 2022 Aug 1.
Published in final edited form as: Nature. 2022 Apr 28;606(7914):585–593. doi: 10.1038/s41586-022-04802-1

Extended data figure 12. CXCL10-associated genes(matched to figure 3).

Extended data figure 12.

a. Network (STRING v11.0) analysis of top CXCL10-associated genes (top 200 genes). K-means clustering. Clusters and their corresponding pathway analysis are available as source files. Top genes that correlate with CXCL10 (4dpi, Pearson and Spearmen correlation combined) are enriched for distinct inflammatory molecules.

b. Network (STRING) analysis of genes that are preferentially associated with CXCL10 but not with TLR7 or TNF. Disconnected nodes in the network are not displayed. K-means clustering. Clusters and their corresponding pathway analysis are presented as source files.

c. Proportions of TNF or CXCL10 producing macrophages among alveolar (CD206hiCD68+) macrophages. Unpaired, two-tailed t-test. N=6 biologically independent mice examined over 3 independent experiments. MISTRG6-hACE2 mice were infected with SARS-CoV-2-mNG and lungs were analyzed at 4dpi.

d. Distribution of CXCL10 or TNF associated genes at 4, 14, 28 dpi in lungs infected with SARS-CoV-2 or not. Analysis performed on macrophages of 4dpi lungs in Fig 3d was extended to more timepoints. Pearson (right) and Spearman (left) correlation values were calculated for each gene for its correlation with CXCL10 or TNF in human monocytes and macrophages isolated from uninfected and infected (4, 14 and 28 dpi) lungs. K-means clustering analysis.