In vivo blockade of IL-17 inhibits inflammatory lymphangiogenesis in Th17-dominant autoimmune DED. DED was induced in wild-type C57BL6 mice by exposing them continuously to a dry air-controlled environment,²  which induces an autoimmune ocular surface disease.⁴  After 4 days of disease induction, mice were randomized into 3 groups receiving topically anti–IL-17 antibody, control isotype antibody, or left untreated. Progression of clinical disease was monitored by corneal fluorescein staining,¹⁸  a readout for clinical signs of dry eye inflammation, from day 0 to day 12, at which time corneas were harvested for immunohistochemical and real-time PCR analyses. (A) Corneas were immunostained with CD31 (green) and Lyve1 (red) antibodies. Digital micrographs using epifluorescence microscopy were captured and ImageJ software was used to (B) quantify the growth of blood (CD31^hiLyve1⁻) and lymphatic (CD31^loLyve1⁺) vessels. (C) Real-time PCR analysis was performed to measure the expression levels of lymphangiogenic-specific VEGF-D and VEGF-C in untreated, isotype Ab-treated, and anti–IL-17 Ab-treated DED corneas. Expression levels of VEGF-D and VEGF-C were normalized to GAPDH levels as an internal control and then with their levels in normal corneas. (D) Corneal fluorescein staining scores showing severity of clinical disease in untreated, isotype, and anti–IL-17 Ab-treated groups. Each group consists of 6 mice. Data are mean ± SEM. *P < .05, by Student t test. n.s. indicates not significant.