Immunological mechanisms play a pivotal role in regulating the ocular surface environment. It was demonstrated that anti-inflammatory factors such as the expression of vascular endothelial growth factor receptor-3 (VEGFR-3) in corneal cells, immature corneal resident antigen-presenting cells and regulatory T cells play an active role in protecting the ocular surface1. In particular, inflammation plays a crucial role for the chronicity of Dry eye disease (DED), its symptoms and its clinical signs. Dry eye symptoms range from mild, transient irritation to persistent dryness, burning, itchiness, redness, pain, ocular fatigue, and visual disturbance; furthermore molecular modifications related to dry eye symptoms are modifications of the structural compartments of the ocular surface and microvilli ‘network’.2

Corneal epithelium is an avascular tissue but keratocytes, and hematopoietic cells respond to inflammation by changing phenotype and Antigen presenting cell APC cells could be trafficking from the eye. Furthermore it is well known that Infraclinical signs od DRY EYE are often associated to the use of preserved eye drops. Moreover, in the case of glaucoma treatment, compliance may be further compromised by the development of ocular surface disease caused, not by the active component of treatment, but by the preservative used to protect it from bacterial contamination6.

In the fig. 1 are reported the major efferent immunoregulatory mechanisms on normal ocular surface and their disruption in dry eye disease.

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