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Ocular surface immune cells are a **heterogeneous group** of innate and adaptive immune cells residing in the tissues that make up the ocular surface—primarily the cornea and conjunctiva. These include **macrophages**, **dendritic cells**, **mast cells**, **T lymphocytes** (including Th1 and Th17 subsets), **B lymphocytes**, neutrophils, natural killer (NK) cells, and plasma cells[3][7][4]. Their primary functions are to protect against pathogens through both innate mechanisms—such as phagocytosis by macrophages or antigen presentation by dendritic/Langerhans’ cells—and adaptive responses mediated by T and B lymphocytes[3][7]. These immune populations play a central role in maintaining ocular health but can also contribute to diseases such as dry eye disease when dysregulated. For example, increased infiltration or altered function of these immune cell types is associated with chronic inflammation on the ocular surface seen in dry eye disease[7][4]. Therapeutic agents like cyclosporine A suppress T-cell activation broadly while lifitegrast specifically blocks LFA‑1/ICAM‑1 interactions involved in recruiting inflammatory T-cells to the ocular surface[4]. However, "ocular surface immune cell" is not a single molecular target but rather refers collectively to multiple distinct cellular entities. Therefore it is not considered a canonical therapeutic target like an individual receptor or enzyme; instead it describes a complex system comprising many targets. Because this entry refers to a broad population rather than one specific molecule or receptor—and thus cannot be mapped directly onto standard drug-target databases—it should be flagged as incorrect for structured target mapping purposes. > As is true with any mucosal tissue, the ocular surface harbors a variety of immune cells of the innate-adaptive continuum...[7] > The interior of the eye lacks lymph vessels but is highly vascularized...many immune cells reside in the uvea...mostly macrophages, dendritic cells and mast cells...[1] > Specifically TH1 and TH17 are primary lymphocyte subtypes involved in damage/inflammation related to DED...They release cytokines that alter normal balance...[4]
Immunosuppression (e.g., inhibition of T cell activation and cytokine production by cyclosporine A[4]) Blockade of LFA‑1/ICAM‑1 interaction to reduce T cell-mediated inflammation (lifitegrast[4])
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