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Dry eye disease (DED) is a common chronic ocular surface disorder that significantly impacts quality of life. Its pathogenesis involves disruption of immune regulatory mechanisms and ocular surface inflammation, which mutually reinforce each other in a vicious cycle. Conventional treatments, such as artificial tears and meibomian gland care, alleviate symptoms but often fail to control underlying inflammation. Anti-inflammatory therapy is therefore crucial. Traditional agents like corticosteroids provide rapid relief but carry risks with long-term use. Cyclosporine A, an immunosuppressant, offers unique advantages by inhibiting T-cell activation, reducing pro-inflammatory cytokines, enhancing tear secretion, and restoring the ocular surface. Clinical and experimental studies have consistently demonstrated its efficacy and safety in improving tear production, relieving symptoms, repairing ocular surface structures, and slowing disease progression. This review summarizes the mechanisms, recent clinical evidence, and future perspectives of topical cyclosporine A in DED treatment, providing a reference for rational clinical use and novel therapeutic development.
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Bian et al. (2025) studied this question.
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