Fig. 1: Human ex vivo and in vitro expanded ILC2s specifically express PPARγ.

a Heatmap of row z-scores of mRNA level of proteins involved in fatty acid metabolism (highlighted in italics) or involved in protein-protein interaction with PPARγ (highlighted in bold). Fatty acid metabolism genes were taken from the “fatty acid metabolic process” Gene Ontology gene set (GO:0006631, http://geneontology.org/). RNA-sequencing counts were transformed to log2 counts per million, and differential gene expression analysis was performed by fitting a linear model to each gene using the voom function in the limma package for R (v. 3.38.3), followed by a moderated t statistic computation using the empirical Bayes statistics model implemented in the limma package (See Ercolano et al.¹ for detailed methods). Genes significantly upregulated in ILC2s compared to ILC1s and/or ILCPs are indicated using an * (n = 3; *P < 0.05). Proteins putatively involved in protein–protein interactions were taken from the STRING database (https://string-db.org/). b Expression of PPARs assessed by qPCR in human freshly sorted ILC subsets (open square ILC1s, open circle ILC2s, open triangle ILCPs) (ILC1s n = 6; ILC2s and ILCPs n = 7; ILC1s vs ILC2s **P = 0.0032, ILC2s vs ILCPs **P = 0.0021). c Expression of PPARs assessed by qPCR in in vitro expanded human ILC subsets (open square ILC1s, open circle ILC2s, open triangle ILCPs) (ILC1s and ILCPs n = 3; ILC2s n = 5; ILC1s vs ILC2s ****P < 0.0001, ILC2s vs ILCPs *P = 0.0020). d Western blot analysis of PPARγ expression at protein level in ILC2s compared to ILC1s and ILCPs (one individual experiment). Each symbol represents one individual donor. Data are shown as mean ± SEM and were analyzed by one- (b) or two-way (c) ANOVA tests. Source data are provided as a Source data file.