Fig. 6. Acute hypoxia exposure delays ILC3 responses in a HIF-1 manner.

A Experimental scheme of HIF-1α^ΔRorc and HIF-1α^floxed mice housed under normoxia or 8% O₂-hypoxia, using a normobaric gas chamber, for 48 h. B Absolute number of ILC subtypes in small intestine lamina propria (n = 3–4). ILC1, ILC2, and ILC3 are defined as Lin^-CD45⁺RORγt^-Gata3^-Nkp46⁺, Lin⁻CD45⁺RORγt⁻Gata3⁺ and Lin⁻CD45⁺RORγt⁺Gata3^-, respectively. C Geometric MFI of T-bet in ILC1, Gata3 in ILC2, T-bet and RORyt in ILC3 from si-lamina propria of HIF-1α^ΔRorc and HIF-1α^floxed mice kept in normoxia or hypoxia (n = 3–4). D Percentage of Ki67⁺ ILC1 (Lin^-Tbet⁺, left) and ILC3 (Lin^-RORγt⁺, right) under normoxia or hypoxia (n = 3–4). Representative FACS plots are presented on the left. E Percentage of IL-22, IL-17, and IFN-γ producing Lin^-CD45^lowCD90.2⁺ (si-ILC3-enriched population) cells from HIF-1α^ΔRorc and HIF-1α^floxed mice in normoxia or hypoxia (n = 3–4). F Relative IL-22-target gene expression in distal ileum under normoxia or hypoxia (n = 4). All HIF-1α^ΔRorc and HIF-1α^floxed mice were littermates and matched by sex and age. Results are presented as mean ± SEM. *p < 0.05; **p < 0.01; ***p < 0.001.