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. Author manuscript; available in PMC: 2015 Feb 2.
Published in final edited form as: Science. 2014 Jan 24;343(6169):432–437. doi: 10.1126/science.1247606

Figure 1. ILC3 are enriched in the GI tract and depend on retinoic acid.

Figure 1

A) Flow cytometric analysis of cells isolated from small intestinal lamina propria (gut), lung and skin of naïve C57Bl/6 mice. Upper panel represents live CD45+ cells stained with Thy1.2 and lineage (lin) markers (NK1.1, TCRβ, TCRγδ, CD11b, CD11c, CD4, CD8a, CD8b, CD19, GR-1, DX5, Ter119). Lower panel displays cells gated on Lin− and Thy1.2 expression (ILC), stained for RORgt (ILC3) and GATA3 (ILC2). B) Frequencies of ILC2 and ILC3 in gut, lung and skin. C) Small intestinal lamina propria (SiLP) cells from control (Ctrl) or vitamin A insufficient (VAI) WT or Rag1−/− mice, gated on Lin−, Thy1.2+ cells and analyzed for GATA3 and RORγt expression. D–E) Total numbers of ILC3 (RORγt+) and ILC2 (GATA3+) cells in the SiLP of WT and Rag1−/− mice. F) Intracellular IL-13 and IL-22 expression in Lin− Thy1.2+ cells following stimulation with PMA and ionomycin and G–H) Total numbers of IL-22 and IL-13 producing ILC in the SiLP. I) SiLP ILC2 and ILC3 from Rag1−/− mice treated with vehicle control (Veh) or retinoic acid receptor inhibitor (RAi) for 8 days and J) Intracellular IL-13 and IL-22 expression in ILC following stimulation with PMA and ionomycin. Results are representative of at least three independent experiments with 3–5 mice in each experimental group. All graphs display means ±SEM.

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