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Inflammation is involved in the pathogenic mechanism of most of the chronic ocular surface disorders. In fact, the ocular surface can be considered as an ‘immunological’ unit that works with the aim to protect the visual system from external and internal noxae. This exposes the ocular surface structures to a continuous, subclinical, inflammatory condition. In this way, the ocular surface acts as an anatomical and functional unit that maintains a controlled immunological protection against several stimuli, such as allergens, chemical or physical irritants, traumas and infections from the external environment. Normally, the ocular surface system can modulate the immunological response to avoid possible negative consequences on its structures due to an ‘exaggerated’ response or chronic activation of the immune system. However, if the pro-inflammatory stimuli are prolonged or strong enough, they can induce morphological and functional ocular surface changes, which may lead to the maintenance of a chronic inflammatory status.1 ,2
Innate and adaptive immunity participate to the defensive systems of the ocular surface. Among the innate mechanisms, the activation of toll-like receptors (TLRs), also due to the modified ocular surface flora, and the increased expression of molecules, such as acidic mammalian chitinase,3 ,4 phospholipase A2 and transglutaminase 2, have been described.1 ,5
The initiation of innate immunity mechanisms via these molecules results in the activation of the mitogen-activated protein kinase and nuclear factor κB signalling pathways, which induce the expression of pro-inflammatory cytokines such as interleukin (IL)-1α, IL-1β, IL-6, IL-17, tumour necrosis factor α, and matrix metalloproteinases.6–10 The expression of these and other molecules, if the irritating …
Competing interests None.
Provenance and peer review Commissioned; internally peer reviewed.
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