Fig. 7

IL-17A is a critical mediator of ATSE-induced delayed wound healing and exacerbated inflammation. a Relative IL-17A expression using mRNA isolated from whole wounded corneas of the RA, ATSE, and ATSE + 6-OHDA groups at 6, 12, 18, and 24 h post-corneal abrasion (one-way ANOVA, Tukey's post hoc test, RA vs. ATSE, *p < 0.05, **p < 0.01, ***p < 0.001; RA vs. ATSE + 6-OHDA, ^##p < 0.01, ^###p < 0.001, n = 4 corneas per time point per group). The data represent three independent experiments. b Representative open corneal wounds (revealed by topical fluorescein) and visible wound closure over time. c Percent decrease in open wound area over time post-wounding (two-way RM ANOVA, interaction p < 0.0001, Bonferroni’s multiple comparisons test, n = 6 corneas per time point per group). d Number of dividing epithelial cells over time post-wounding (two-way AVOVA, interaction p = 0.00047, Sidak’s multiple comparisons test, n = 6 corneas per time point per group). e Neutrophil influx into the cornea over time after corneal abrasion (two-way ANOVA, interaction p < 0.0001, Sidak’s multiple comparisons test, n = 6 corneas per time point per group). f γδ T cell influx into the cornea over time after corneal abrasion (two-way ANOVA, interaction p = 0.31888, Sidak’s multiple comparisons test, n = 6 corneas per time point per group). *comparison between the ATSE + isotype IgG and RA + isotype IgG groups with *p < 0.05, **p < 0.01, and ***p < 0.001; ^#comparison between the ATSE + isotype IgG and ATSE + mAb IL-17A groups with ^#p < 0.05, ^##p < 0.01, and ^###p < 0.001