Figure 1
From: Chronic dry eye disease is principally mediated by effector memory Th17 cells
Chronic dry eye disease (DED) involves immunoinflammatory responses at the ocular surface. (a) Development of chronic DED. Acute DED was induced in mice by desiccating stress for 14 days. Subsequently, mice were transferred to the normal vivarium without anti-cholinergic challenge and observed until day 126. Low-level corneal epitheliopathy persisted as evidenced by a slight elevation in corneal fluorescein staining (CFS) scores (solid blue line), which were evaluated in a masked fashion. Meanwhile, aqueous tear production, as assessed with the cotton thread test, returned to normal or even to supra-normal levels (solid pink line). Age- and sex-matched mice maintained in the standard environment were used as normal controls with mean levels of CFS scores and tear production shown in dashed blue and pink lines, respectively. Data shown represent the mean±s.e.m. of a single trial (n=10 eyes) out of two performed. (b) Representative CFS images of normal, acute DED (day 14), and chronic DED (day 126). (c) Relative quantification of interferon (IFN)-γ and interleukin (IL)-17 mRNA levels in the conjunctiva. Data represent the mean±s.e.m. of six eyes per group from a single experiment that was reproduced in a similar independent experiment. *P<0.05; **P<0.01. (d) Representative whole-mount corneal immunofluorescence micrographs demonstrating lymphangiogenesis in DED. Corneas were stained with CD31 (green) and LYVE-1 (red) to evaluate blood (CD31hiLYVE-1−) and lymphatic (CD31loLYVE-1+) vessels. Bars=50 μm. The corneal area covered by lymphatic vessels were quantified using Fiji software and presented in a bar graph. *P<0.05; **P<0.01.
