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The term "inflammatory mediators at the ocular surface" refers collectively to a diverse set of molecules—including cytokines (e.g., interleukin 1β [IL‑1β], interleukin 6 [IL‑6], tumor necrosis factor alpha [TNF‑α]), chemokines, matrix metalloproteinases (MMPs), and neuropeptides—that orchestrate immune responses and drive inflammation in tissues covering the eye such as the cornea and conjunctiva. These mediators are produced by both resident cells of the ocular surface epithelium and infiltrating immune cells during conditions like dry eye disease or allergic conjunctivitis. Their upregulation leads to tissue damage through disruption of epithelial barriers, loss of mucin-producing goblet cells, nerve injury, gland dysfunction, and chronic symptoms associated with diseases like dry eye or keratoconus[2][3][7]. While individual molecules within this group can be considered therapeutic targets—such as IL‑17A or TNF‑α—the phrase itself does not denote a specific druggable entity but rather an entire class involved in pathological processes.
Mechanisms include inhibition of cytokine production/release or immune cell infiltration.
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