During the 1-year follow-up, the combination of OK and atropine 0.01% ophthalmic solution was more effective in slowing axial elongation than OK monotherapy in children with myopia.

Eighty Japanese children, aged 8-12 years, with a spherical equivalent refraction (SER) of − 1.00 to − 6.00 dioptres (D) were randomly allocated into two groups to receive either a combination of orthokeratology (OK) and 0.01% atropine solution (combination group) or monotherapy with OK (monotherapy group). Seventy-three subjects completed the 2-year study. Over the 2 years, axial length increased by 0.29 ± 0.20 mm (n = 38) and 0.40 ± 0.23 mm (n = 35) in the combination and monotherapy groups, respectively (P = 0.03). Interactions between combination treatment and age or SER did not reach significance level (age, P = 0.18; SER, P = 0.06). In the subgroup of subjects with an initial SER of − 1.00 to − 3.00 D, axial length increased by 0.30 ± 0.22 mm (n = 27) and 0.48 ± 0.22 mm (n = 23) in the combination and monotherapy groups, respectively (P = 0.005). In the − 3.01 to − 6.00 D subgroup, axial length increased by 0.27 ± 0.15 mm (n = 11) and 0.25 ± 0.17 mm (n = 12) in the combination and monotherapy groups, respectively (P = 0.74). The combination therapy may be effective for slowing axial elongation, especially in children with low initial myopia. The prevalence of myopia is increasing worldwide 1-3 and younger generations are affected more than others 4-6. Myopia progression in children is strongly associated with axial elongation 7. Retinal changes caused by axial elongation of high myopia increase the risks of myopic maculopathy, retinal detachment, glaucoma, and resulting blindness 4,8,9. Although controlling axial elongation is vital for reducing the risk of these complications, no treatment has yet been established to halt axial elongation. Recent studies, however, have provided evidence of effective methods to slow the progression of myopia. The Atropine for the Treatment of Myopia (ATOM) 1 study demonstrated that treatment with 1% atropine ophthalmic solution significantly suppressed the progression of myopia by about 80% compared to placebo over a 2-year period 10. However, 1% atropine produced secondary unwanted effects such as pupil dilation and loss of accommodation 11 , and rebound effect after cessation of treatment 12. Thus, in the ATOM2 study, 0.5%, 0.1%, and 0.01% atropine ophthalmic solutions were examined, leading to reduced myopia progression by about 75%, 70%, and 60%, respectively, compared to placebo in the ATOM1 study over a 2-year period 13-15. Because the secondary unwanted effects and rebound effect were scarcely seen in the 0.01% atropine group compared to the higher concentrations of atropine, 0.01% atropine was the most recommended. However, axial elongation was not suppressed significantly in the ATOM2 study. Recently, the low-concentration atropine for myopia progression (LAMP) study compared the efficacy of 0.05%, 0.025%, and 0.01% atropine ophthalmic solutions and placebo for suppressing myopia progression and axial elongation 16,17. The results showed that 0.05% atropine was the most effective for suppressing of myopia progression and axial elongation with tolerable secondary un...

The eye is an immune-privileged organ, and corneal transplantation is therefore one of the most successful organ transplantation. The immunosuppressive intraocular microenvironment is known as one of the mechanisms underlying immune privilege in the eye. T-cell immunoglobulin and mucin domain (Tim)-3 is a regulatory molecule for T-cell function, and galectin (Gal)-9 is a Tim-3 ligand. We investigated the role of this pathway in establishing the immune-privileged status of corneal allografts in mice. Gal-9 is constitutively expressed on the corneal epithelium, endothelium and iris-ciliary body in normal mouse eyes and eyes bearing surviving allografts, and Tim-3 was expressed on CD8 T cells infiltrating the allografts. Allograft survival in recipients treated with anti-Tim-3 monoclonal antibody (mAb) or anti-Gal-9 mAb was significantly shorter than that in control recipients. In vitro, destruction of corneal endothelial cells by allo-reactive T cells was enhanced when the cornea was pretreated with anti-Gal-9 mAb. Blockade of Tim-3 or Gal-9 did not abolish anterior chamber-associated immune deviation. We propose that constitutive expression of Gal-9 plays an immunosuppressive role in corneal allografts. Gal-9 expressed on corneal endothelial cells protects them from destruction by allo-reactive T cells within the cornea.