PURPOSE. Dry eye is a major ocular pathology worldwide. Although dry eye is a multifactorial disease, recent studies have shown that chronic immunologic processes have a pivotal role in its pathogenesis, characterized by the infiltration of immune cells in the lacrimal glands, elevated levels of tear inflammatory cytokines, and increased density of immune cells in the cornea and conjunctiva. This review describes the recent advances in understanding the relationship between dry eye and inflammation. METHODS. This narrative review is based on searches of recent international literature using terms related to the immune response in dry eye, and includes clinical trials, animal experiments, and expert reviews. RESULTS. Although dry eye presents clinically as tear film instability associated with corneal/ conjunctival epithelial disorders, Meibomian gland dysfunction, and decreased visual function, recent laboratory and clinical studies have indicated inflammation in the lacrimal glands, Meibomian glands, conjunctiva, cornea, and aqueous tears. Furthermore, inflammation at these locations leads to conjunctival goblet cell apoptosis, corneal epithelial barrier disruption, and corneal nerve damage. These inflammatory outcomes can be exacerbated by intrinsic and extrinsic factors, such as aging, sex steroid hormone, autoimmune diseases, contact lens use, visual display terminals, and dry environment. CONCLUSIONS. Recent advances in dry eye research have revealed the inflammatory process and its pathogenesis, which has been proposed as an ''inflammatory vicious cycle'' of dry eye. Comprehensive assessment of dry eye based on inflammation will improve the selection of treatments and help break the inflammatory cycle in clinical settings.

Proinflammatory tear cytokines are elevated bilaterally in patients with unilateral BK, and are correlated strongly with alterations in DCs and nerve density as detected by IVCM.

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Postoperative endothelial cell loss leads to graft failure after corneal transplantation, and is one of the important issues for long-term prognosis. The objective of this study was to identify clinical factors affecting graft survival and postoperative endothelial cell density (ECD) after Descemet’s stripping automated endothelial keratoplasty (DSAEK). A total of 198 consecutive Japanese patients (225 eyes) who underwent DSAEK were analysed using Cox proportional hazard regression and multiple linear regression models. The candidate factors included recipient age; gender; diagnosis; pre-existing iris damage state, scored based on its severity; the number of previous intraocular surgeries; graft ECD; graft diameter; simultaneous cataract surgery; surgeons experience; intraoperative iris damage; postoperative rebubbling; and graft rejection. Eyes with higher pre-existing iris damage score and more number of previous intraocular surgery had a significantly higher risk of graft failure (HR = 8.53; P < 0.0001, and HR = 2.66; P = 0.026, respectively). Higher pre-existing iris damage score, lower graft ECD, and smaller graft diameter were identified as significant predisposing factors for lower postoperative ECD. The results show that iris damage status before DSAEK may be clinically useful in predicting the postoperative course. Avoiding intraoperative iris damage, especially in eyes with low ECD can change the prognosis of future DSAEK.

A better midterm clinical outcome was achieved with COMET of a substrate-free cell sheet than with COMET of AM as a substrate for treating severe stem cell deficiency.

Postoperative BCVA correlated with irregularity of the anterior surface but not the posterior surface. In addition to corneal transparency, regularity of the anterior surface is an important factor in visual acuity after DSEK.

Posterior surfaces compensate for anterior aberrations in normal, PK, and DALK eyes. In DSAEK eyes, the posterior surface increased total corneal HOAs and had a negative influence on MTFs.

The cornea is the shield to the foreign world and thus, a primary site for peripheral infections. However, transparency and vision are incompatible with inflammation and scarring that may result from infections. Thus, the cornea is required to perform a delicate balance between fighting infections and preserving vision. To date, little is known about the specific role of antigen-presenting cells in viral keratitis. In this study, utilizing an established murine model of primary acute herpes simplex virus (HSV)-1 keratitis, we demonstrate that primary HSV keratitis results in increased conventional dendritic cells (cDCs) and macrophages within 24 hours after infection. Local depletion of cDCs in CD11c-DTR mice by subconjuntival diphtheria toxin injections, led to increased viral proliferation, and influx of inflammatory cells, resulting in increased scarring and clinical keratitis. In addition, while HSV infection resulted in significant corneal nerve destruction, local depletion of cDCs resulted in a much more severe loss of corneal nerves. Further, local cDC depletion resulted in decreased corneal nerve infection, and subsequently decreased and delayed systemic viral transmission in the trigeminal ganglion and draining lymph node, resulting in decreased mortality of mice. In contrast, sham depletion or depletion of macrophages through local injection of clodronate liposomes had neither a significant impact on the cornea, nor an effect on systemic viral transmission. In conclusion, we demonstrate that corneal cDCs may play a primary role in local corneal defense during viral keratitis and preserve vision, at the cost of inducing systemic viral dissemination, leading to increased mortality.