Fig. 2: IL-27 disturbs lipid metabolism and restrains the generation of phospholipids in γδ T17 cells.
a, b RNA-sequencing analysis was performed using in vitro differentiated γδ T17 cells from the spleen of Cd2-Cre Il27raflox/flox or Cd2-Cre mice. GSEA analysis of genes in lipid metabolic process (a) and lipid homeostasis (b) were shown. c Immunoblotting of in vitro differentiated γδ T17 cells from the spleen of Cd2-Cre Il27raflox/flox or Cd2-Cre mice (n = 3). d–g Lipids were extracted from in vitro differentiated γδ T17 cells from the spleen of Cd2-Cre Il27raflox/flox or Cd2-Cre mice and used for lipidomic analysis via LC-MS (n = 6). d Pie chart showing the proportions of each type of lipid component. TG triglyceride, So sphingosine, SM Sphingomyelin, PS Phosphatidylserine, PI phosphatidylinositol, PEt Phosphatidylethanol, PE phosphatidylethanolamines, PC phosphatidylcholine, LPE Lyso phosphatidyl ethanolami, LPC Lyso phosphatidylcholine, dMePE Dimethylphosphatidyleth anolamine. e, f Metabolite set enrichment analysis of significantly altered lipids involved in lipolysis (e) and glycerophospholipids (f). g Heatmap of significantly altered phospholipids belonging to PC, PE and PI. h Flow cytometry analysis of IL-17 in γδ T cells from Cd2-Cre and Cd2-Cre Il27raflox/flox mice that were cultured under γδ T17 priming condition with or without Forskolin (10 μM) (n = 4). Data were presented as mean ± SEM, statistical differences were performed using One-way ANOVA (h). **p < 0.01, ***p < 0.001.
