Immunopathology of Allergic Conjunctivitis

Allergic conjunctivitis is predominantly an immunoglobulin E-mediated hypersensitivity reaction to environmental allergens. Allergic diseases affect >30% of the world’s population, of which 40% report associated ocular manifestations. Cellular and soluble mediators play a major role in the pathophysiology of allergic conjunctivitis. Mast cells, which are major effector cells of allergic conjunctivitis, undergo activation and degranulation to release histamine, tryptase, prostaglandins, leukotrienes, and cytokines. These mediators play important roles in immunopathological mechanisms that generate the clinical manifestations of allergic conjunctivitis. These clinical features include conjunctival hyperaemia, chemosis, tearing, itching, papillae, mucus discharge, and eyelid oedema. Histamine mediates the early phase of the allergic immune response, whereas lipid mediators and cytokines are involved in the late phase of the immunopathology of allergic conjunctivitis. Current management of allergic conjunctivitis includes non-pharmacological approaches such as allergen avoidance and palliative therapy, whereas pharmacological therapeutic modalities may include antihistamine–mast cell stabiliser combination ophthalmic formulations and allergen-specific immunotherapy. Furthermore, as cellular and soluble mediators play a pivotal role in the immunopathogenesis and immunopathology of allergic conjunctivitis, development of immunotherapeutic and pharmacotherapeutic agents specific to these mediators can enhance the therapeutic index and safety profile of anti-allergy treatment.