Fig. 3: The lack of PD-1 signaling upregulates glycolysis in aILC2s.

a–i ILC2s were sorted from WT and PD-1 KO mice after three intranasal challenges with 0.5 μg of rm-IL-33. Sorted cells were incubated with rm-IL-2 (10 ng mL⁻¹) and rm-IL-7 (10 ng mL⁻¹) for 24 h. a Heat map representation of differentially regulated genes involved in the metabolism of aILC2 from WT and PD-1 KO mice. GSA algorithm was used to test for differential expression of genes (p-value < 0.05, n = 3). b Representative histogram (left) of 2-NBDG uptake and the corresponding quantification (right) presented as MFI in FACS-sorted WT and PD-1 KO aILC2s; n = 4. c–f Relative levels of metabolites in the glycolysis pathway analyzed using an LC-MS/MS system. g Measurement of the Oxygen consumption rate (OCR) under basal conditions and in response to indicated drugs. h Cell energy phenotype presented as OCR against extracellular acidification rate (ECAR). i Glycolytic capacity calculated as the difference between maximal and basal ECAR. Data are presented as means ± SEM (n = 3; two-tailed Student’s t test).