Dry eye disease (DED) is increasingly recognized as a condition driven by immune dysregulation at the ocular surface (OS). Chronic inflammation, mediated by aberrant activation of both innate and adaptive immune pathways, underlies disease progression and symptom persistence. Neuroimmune interactions further amplify OS inflammation, contributing to epithelial damage and impaired homeostatic regulation. This review summarizes current literature on the immunopathogenesis of DED, highlighting the complex interplay of molecular mechanisms of innate and adaptive immune activation, neuroimmune-mediated inflammation, and emerging molecular and cellular biomarkers. In addition, we examine existing and emerging therapeutic strategies that target these immune-molecular pathways, including precision immunomodulatory approaches, to inform future management of DED. By integrating mechanistic insights with clinical findings, this review aims to provide a comprehensive overview of the molecular mechanisms underlying the dysregulated immune response associated with DED.

The corneal epithelium, comprising three layers of cells, represents the outermost portion of the eye and functions as a vital protective barrier while concurrently serving as a critical refractive structure. Maintaining its homeostasis involves a complex regenerative process facilitated by the functions of the lacrimal gland, tear film, and corneal nerves. Crucially, limbal epithelial stem cells located in the limbus (transitional zone between the cornea and the conjunctiva) are instrumental for the corneal epithelium integrity by replenishing and renewing cells. Re-epithelialization failure results in persistent defects, often associated with various ocular conditions including diabetic keratopathy. The insulin-like growth factor (IGF) system is a sophisticated network of insulin and other proteins essential for numerous physiological processes. This review examines its role in maintaining the corneal epithelium homeostasis, with a special focus on the interplay with corneal limbal stem cells and the potential therapeutic applications of the system components.

Pseudoexfoliation syndrome (PXS) is an age-related fibrillopathy where fibrillar exfoliation material accumulates and deposits in ocular and extra-ocular tissue. Within the eye, this substance accumulates on the ocular surface and in the anterior segment of the eye, impacting ocular structures such as the conjunctiva, Tenon’s capsule, sclera, cornea, iris, ciliary body, trabecular meshwork, and lens. This review aims to collate the current literature on how each anatomical part of the eye is affected by PXS, with a strong focus on molecular changes. We also summarise the current understanding of the key genetic factors influencing the development of PXS.

The cornea is an avascular, immune-privileged tissue critical to maintaining transparency, optimal light refraction, and protection from microbial and immunogenic insults. Corneal neovascularization (CoNV) is a pathological sequela of multiple anterior segment diseases and presents a major cause for reduced visual acuity and overall quality of life. Various aetiologies, including infection (e.g., herpes simplex), inflammation (e.g., infective keratitis), hypoxia (e.g., contact lens overuse), degeneration (e.g., chemical burns), and trauma, disrupt the homeostatic avascular microenvironment, triggering an overactive compensatory response. This response is governed by a complex interplay of pro- and anti-angiogenic factors. This review investigates the potential for these mediators to serve as therapeutic targets. Current therapeutic strategies for CoNV encompass topical corticosteroids, anti-VEGF injections, fine-needle diathermy, and laser modalities including argon, photodynamic therapy and Nd:YAG. Emerging therapies involve steroid-sparing immunosuppressants (including cyclosporine and rapamycin), anti-fibrotic agents and advanced drug delivery systems, including ocular nanosystems and viral vectors, to enhance drug bioavailability. Adjunctive therapy to attenuate the protective corneal epithelium prior to target neovascular plexi are further explored. Gene-based approaches, such as Aganirsen (antisense oligonucleotides) and CRISPR/Cas9-mediated VEGF-A editing, have shown promise in preclinical studies for CoNV regression and remission. Given the multifactorial pathophysiology of CoNV, combination therapies targeting multiple molecular pathways may offer improved visual outcomes. Case studies of CoNV highlight the need for multifaceted approaches tailored to patient demographics and underlying ocular diseases. Future research and clinical trials are essential to elucidate optimal therapeutic strategies and explore combination therapies to ensure better management, improved treatment outcomes, and long-term remission of this visually disabling condition.

Dry eye disease is increasingly recognised as a condition driven by immune dysregulation at the ocular surface. Chronic inflammation, mediated by aberrant activation of both innate and adaptive immune pathways, underlies disease progression and symptom persistence. Neuroimmune interactions further amplify ocular surface inflammation, contributing to epithelial damage and impaired homeostatic regulation. This review synthesizes current literature on the immunopathogenesis of dry eye disease (DED), highlighting the complex interplay of molecular mechanisms of innate and adaptive immune activation, neuroimmune-mediated inflammation, and emerging molecular and cellular biomarkers. In addition, we examine existing and emerging therapeutic strategies that target these immune-molecular pathways, including precision immunomodulatory approaches, to inform future management of DED. By integrating mechanistic insights with clinical findings, this review aims to provide a comprehensive overview of the molecular mechanisms underlying the dysregulated immune response associated with DED.

The cornea relies on a healthy endothelium to maintain transparency, and damage to endothelial cells can result in corneal oedema and vision loss. Current treatments, which often involve the use of donor corneas, face significant limitations due to a shortage of donor tissue. Although human corneal endothelial cells (HCECs) can be cultured and transplanted, their low attachment rates limit the effectiveness of these treatments. In this review, we examined studies that explore the use of magnetic nanoparticles (MNPs) to enhance the attachment of HCECs to the cornea. We evaluated the effectiveness, cell viability, and safety of this approach. Findings indicate that MNPs facilitate the targeted delivery of HCECs under a magnetic field, resulting in improved corneal clarity and reduced oedema in animal models. Cell viability remained high, and no significant safety concerns were identified. MNPs present a promising strategy to enhance HCEC transplantation. However, further research, including ongoing clinical trials, is necessary to confirm the safety and efficacy of this approach before it can be adopted for widespread clinical use.