Fig. 1

Gluten drives CD3⁺ IEL accumulation, epithelial MHCII expression, unconventional MHCI molecules, and IL-15 upregulation in the absence of IL-10 signaling. Itgax^creIl10ra^fl/fl mice and littermates were reared on a gluten-containing (conventional) or gluten-free diet (GFD) until sacrifice. a CD3 immunohistochemistry on duodenal sections. Scale bar, 100 µm; representative of n = 9–21. b Small intestinal CD45⁺CD3⁺ IEL number from Itgax^creIl10ra^fl/fl mice and littermates obtained by assessing the frequency of single CD45⁺CD3⁺ IEL by flow cytometry and multiplying it to the total cell number of the small intestine IEL fraction. c Ki67 immunohistochemistry on duodenal sections. Scale bar, 100 µm; representative of n = 9–21. d Crypt/villus ratio in Ki67-stained sections. e MHCII expression on small intestine single CD45^neg cells; representative of n = 6–14. f Geometric mean fluorescence intensity (MFI) of MHCII on single small intestinal CD45^neg cells. g–i Quantitative real-time PCR (qRT-PCR) of stress-associated epithelial molecule genes (g, h) or Il15 (i) in sorted live single small intestinal CD45^negEpCAM⁺ cells. Twelve (a), 11 (b-d), 9 (e-f), or 7 independent experiments (g-i). Each square represents one mouse. One-way ANOVA/Bonferroni post-test (d, f: mean + SEM; b, g-i: mean + SD)