Fig. 5: The role of RAGE-TLR4 crosstalk in dAGEs-induced allergic inflammation. | Nature Communications

Fig. 5: The role of RAGE-TLR4 crosstalk in dAGEs-induced allergic inflammation.

From: Dietary advanced glycation end-products promote food allergy by disrupting intestinal barrier and enhancing Th2 immunity

Fig. 5

To elucidate the role of RAGE/TLR4-signaling in food allergic responses manipulated by dAGEs, the adjuvant-free model of food allergy was re-performed in wild type (WT), RAGE-knockout (RAGE−/−), and TLR4-knockout (TLR4−/−) mice. a Schematic illustration of the study design#. b Clinical allergy score of mice upon last challenge. c Rectal temperature change after last challenge. d Serum OVA-specific IgE level. e Serum OVA-specific IgG1 level. f Serum OVA-specific IgG2a level. g–i Representative cell sorting plots and quantification of Th1 and Th2 cells in MLN lymphocytes by flow cytometry. j Interplay between RAGE and TLR4-signaling pathways#. k Relative expression levels of genes related to receptor-mediated signaling in the intestine. Bar graphs show mean ± SEM (k) and boxplots represent median with 25th/75th percentiles (box) and 1.5 × IQR (whiskers) (b–h). n = 5–6. Pair-wise comparison was conducted by Student’s t tests or Mann–Whitney tests (two-tailed). *p < 0.05, **p < 0.01, ***p < 0.001. BSA-AGE methylglyoxal-glycated bovine serum albumin, dAGEs dietary advanced glycation end-products, OVA ovalbumin. #Created in BioRender. Zhang (2025) https://BioRender.com/pf8iqnb. Source data are provided as a Source Data file.

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