Figure 4. Vitamin A deficiency increases ILC2 mediated immunity to helminth infections.

A). Small intestine histologic sections of Ctrl, VAI or VAI Rag1^−/− mice treated with anti-IL13 antibody (VAI+αIL13) stained with PAS to visualize goblet cells. B) Total numbers of PAS-positive goblet cells per crypt and C) Retnlb (Relm-β) gene expression in the small intestine of Ctrl, VAI or VAI+αIL13 Rag1^−/− mice. D) Lamina propria ILC2 and ILC3 isolated from the cecum of Ctrl or VAI WT mice 13 days after oral infection with T. muris (upper panel) and intracellular IL-13 and IL-22 expression in ILC after stimulation with PMA and ionomycin (lower panel). E) Total numbers of ILC2 and F) total numbers of IL-13 producing ILC in the cecum. G) Worm burden in the cecum of Veh, RAi, RAi treated IL-13^−/− (RAi IL-13^−/−) and RAi mice treated with neutralizing anti-IL13 antibody (RAi a-IL13) 12 days after infection. H) Number of worms in Ctrl and VAi Rag1^−/− mice 12 days after infection and I) intracellular GATA3 and RORγt (upper panel) and IL-13 and IL-22 expression (lower panel) in cecal ILC. J) Total numbers of ILC2 and IL-13⁺ ILC in the cecum of T. muris infected mice. Data represents at least two (A–B, H–J) or three (D–G) independent experiments with 3–5 mice in each experimental group. Data in G) Veh and RAi is pooled from three experiments, RAi a-IL13 and RAi IL-13^−/− represent one experiment each. All graphs display means ±SEM.