Topical CsA could be an effective treatment for DES, especially for DES associated with conjunctival injury. Further RCTs with larger sample sizes for different clinical types of DES are warranted to determine the efficacy and limitation for different clinical types of DES.

The use of intraoperative topical MMC 0.02% for 15 seconds after LASEK did not affect the corneal endothelium.

The aim of this study was to explore whether IL-7 participates in the pathogenesis of Graves' ophthalmopathy (GO). This was a prospective study. 20 GO patients (40 eyes) and 20 healthy volunteers (40 eyes) were recruited. The tear concentration of IL-7 was measured using ELISA assay. IL-7 expression in orbital tissues was evaluated by immunohistochemistry. Patients with inactive GO had the highest IL-7 concentrations in the tears, followed by healthy controls and patients with active GO per ELISA. Immunohistochemistry analysis showed that IL-7 expression in orbital tissues of the inactive GO samples was higher than that of the volunteers. Changes of IL-7 expression in different phases of GO suggested that IL-7 may play an important role in the pathogenesis of GO.

CD34(+) fibrocytes are bone marrow-derived monocyte progenitor cells that traffic to sites of tissue injury and repair. They putatively infiltrate the orbit in thyroid-associated ophthalmopathy where they appear to transition into CD34(+) orbital fibroblasts (OFs) that interact with residential CD34(-) fibroblasts. A unique phenotypic attribute of fibrocytes and CD34(+) OFs is their expression of the functional thyrotropin receptor (TSHR) and other "thyroid-specific" proteins. When activated through TSHR, fibrocytes express a number of cytokines and other inflammatory genes. Here we sought to determine whether pentraxin-3 (PTX-3), an acute-phase protein involved in inflammation and autoimmunity, might be induced by TSH in fibrocytes and OFs. These cells were collected from patients with Graves disease and healthy individuals. PTX-3 mRNA levels were determined by real-time PCR, protein was determined by ELISA and Western blot, and PTX-3 gene promoter activity was assessed with reporter assays. PTX-3 expression was induced by TSH in both cell types, regardless of the health status of the donor and was a consequence of increased steady-state PTX-3 mRNA levels. M22, a TSHR-activating monoclonal antibody, also induced PTX-3. The induction could be attenuated by dexamethasone and by IGF-I receptor-blocking antibodies, teprotumumab and 1H7. TSH effects were mediated through phosphatidylinositol 3-kinase/AKT, mammalian target of rapamycin/p70(s6k), Janus tyrosine kinase 2 pathways, and enhanced PTX-3 mRNA stability. These findings indicate that PTX-3 is a TSH target gene, the expression of which can be induced in fibrocytes and OFs. They suggest that PTX-3 might represent a previously unidentified nexus between the thyroid axis and the mechanisms involved in tissue remodeling.