The functional role of Langerhans cells (LCs) in ocular surface inflammation and nerve damage in dry eye (DE) disease has yet to be determined. This study was performed to investigate this relationship through both clinical study on DE patients and in vivo mouse models with induced DE disease. In a cross-sectional case-control study (54 eyes of DE patients; 34 eyes of control patients), average cell density, area, and process length of LCs were measured using confocal microscopy. Data were analyzed to determine whether changes in LCs are correlated with subbasal nerve plexus (SNP) parameters (nerve density, beading, and tortuosity). In DE patients, SNP density marginally decreased and nerve beading and tortuosity were significantly increased compared to the control group. The total number of LCs significantly increased in DE patients, and some LCs with elongated processes were found to be attached to nerve fibers. Interestingly, nerve loss and deformation were correlated with inactivation of LCs. In an in vivo experiment to elucidate the role of LCs in ocular surface inflammation and corneal nerve loss, we used a genetically modified mouse model (CD207-DTR) that reduced the population of CD207 (Langerin) expressing cells by injection of diphtheria toxin. In CD207-depleted mice with DE disease (CD207-dDTR+DE), corneal nerves in the central region were significantly decreased, an effect that was not observed in wild-type (WT)+DE mice. In CD207-dDTR+DE mice, infiltration of CD4+, CD19+, CD45+, and CD11b+ cells into the ocular surface was increased, as confirmed by flow cytometry. Increased IL-17 and IFN-γ mRNA levels, and decreased expression of neurotrophic factors and neurotransmitters, were also found in the CD207-dDTR+DE mice. These data support a functional role for LCs in negatively regulating ocular surface inflammation and exhibiting a neuroprotective function in DE disease.

Objectives To compare and evaluate the characteristics of hypertensive choroidopathy with serous retinal detachment in preeclampsia and malignant hypertension (HTN) and explore choroidal ischemia as a pathogenesis using multimodal imaging. Methods A retrospective multicenter case series. Medical charts were reviewed. Clinical characteristics and multimodal imaging, including optical coherence tomography (OCT) and OCT angiography (OCTA), were evaluated. Results Fifty-three eyes of 29 preeclampsia patients and 45 eyes of 24 HTN patients were included. There were no differences in age, follow-up duration, baseline visual acuity, central macular thickness (CMT), or subfoveal choroidal thickness (CT) between the two groups. Blood pressure parameters, including systolic blood pressure, diastolic blood pressure, and pulse rate, were significantly higher in the HTN group. After serous retinal detachment resolved, both CMT (p < 0.001) and CT (p = 0.003) decreased more in the preeclampsia group. Hypertensive retinopathy features, including hemorrhage, exudates, cotton-wool spots, and optic disc edema, were predominantly found in the HTN group (p = 0.001). Final visual acuity was better in the preeclampsia group than in the HTN group (p = 0.048). Poor visual prognostic factors included the presence of retinopathy features (p = 0.005) and retinal detachment in the macula (p = 0.017). Conclusion Choroidal circulation may be affected earlier than retinal circulation by elevated blood pressure, presumably because of anatomical differences and autoregulatory mechanisms in the retinal vasculature. Serous retinal detachment with hypertensive choroidopathy presented with choroidal thickening that decreased after resolution, but the residual flow defects observed in the choriocapillaris on OCTA confirmed the long-hypothesized notion that ischemia is a mechanism underlying hypertensive choroidopathy.

We aimed to investigate the efficacy and safety of primary retropupillary iris claw intraocular lens (R-IOL) implantation in patients with complete intraocular lens (IOL) dislocation. In this single-center retrospective case series, we reviewed the medical records of patients who underwent R-IOL implantation surgery with pars plana vitrectomy for the treatment of IOL dislocation between September 2014 and July 2019. The primary outcome was change in visual acuity (VA) up to 24 months postoperatively. The secondary outcomes included changes in intraocular pressure (IOP), refractive errors, and endothelial cell count (ECC) over the same period. Data of 103 eyes (98 patients) were analyzed. The mean uncorrected VA was significantly improved at one month postoperatively (− 0.69 logMAR, P < 0.001), compared to the preoperative value. IOP (− 2.3 mmHg, P = 0.008) and ECC (− 333.4 cells/mm2, P = 0.027) significantly decreased one month post-surgery and remained stable thereafter. Postoperative mean spherical equivalents were similar to the prediction error throughout the follow-up period. IOP elevation (n = 8, 7.8%), cystoid macular edema (n = 4, 3.9%), and dislocation of the R-IOL (n = 10, 9.7%) were managed successfully. Overall, primary R-IOL implantation with pars plana vitrectomy is effective and safe for correcting IOL dislocation due to various causes.