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Mast cells are specialized immune cells of the myeloid lineage that reside in mucosal and epithelial tissues, including the conjunctiva of the eye [1]. They are central mediators of type I hypersensitivity reactions, characterized by the release of pre-formed inflammatory mediators such as histamine, heparin, and proteases (e.g., tryptase) through a process called degranulation [2]. This activation typically occurs when allergens cross-link IgE antibodies bound to the high-affinity FcεRI receptors on the mast cell surface [3]. In the conjunctiva, mast cell degranulation leads to the clinical manifestations of allergic conjunctivitis, including itching, redness, and edema [4]. Therapeutic agents known as mast cell stabilizers, such as cromolyn sodium and lodoxamide, are used to prevent the release of these mediators, thereby managing allergic symptoms [5]. While mast cells are essential for host defense against parasites and toxins, their overactivation or proliferation is associated with diseases like asthma, anaphylaxis, and mastocytosis [6].
Mast cell stabilizers inhibit the degranulation of mast cells, preventing the release of histamine and other inflammatory mediators. This is thought to occur through the stabilization of the cell membrane or the modulation of chloride channels and G-protein coupled receptors like GPR35 [1, 5].
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