Fig. 4 | Cellular & Molecular Immunology

Fig. 4

From: A de novo missense mutation in MPP2 confers an increased risk of Vogt–Koyanagi–Harada disease as shown by trio-based whole-exome sequencing

Fig. 4

Increased expression of inflammatory-related proteins after MPP2-N315 mutation. A The volcanic map of DEGs in MPP2-K315 or MPP2-N315 mutant ARPE19 cells. B The volcanic map of DEGs in MPP2 wild-type or mutant mice with EAU. C, D GO enrichment analysis of proteomics in vitro and in vivo. E, F Protein levels and quantitative charts of ERK3, ERK1/2, NF-κB p65, and p-STAT3 in vitro (n = 3/group; mean ± SD; **p < 0.01; one-way ANOVA). G, I Protein expression and quantification of ERK3, ERK1/2, NF-κB p65 and p-STAT3 in PBS, vehicle, MPP2-K315 or MPP2-N315 AAV-administered mice with EAU modeling (n = 3/group; mean ± SD; ** p < 0.01; one-way ANOVA). H, J Protein levels and quantitative graphs of ERK3, ERK1/2, NF-κB p65 and p-STAT3 in MPP2-K315 or homozygous or heterozygous MPP2-N315 knock-in mice with immunization (n = 3/group; mean ± SD; *p < 0.05; one-way ANOVA). K The extracellular protein level of IL-17E (n = 6/group; mean ± SD; **p < 0.01; one-way ANOVA). L The secretion level of IL-17E in mice with EAU treated with PBS, vehicle, MPP2-K315 or MPP2-N315 AAV (n = 6/group; mean ± SD; *p < 0.05, **p < 0.01; one-way ANOVA). M The secretion of IL-17E in MPP2-K315 or homozygous or heterozygous MPP2-N315 knock-in mice with immunization (n = 6/group; mean ± SD; *p < 0.05, **p < 0.01; one-way ANOVA)

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