Dry eye syndrome, (DE), also known as dysfunctional tear syndrome (DTS), is an inflammatory condition of the ocular surface derived by tear hyperosmolarity consequent to either increased tear evaporation (EDE) or aqueous deficiency (ADDE). Several external stimuli continuously trigger the ocular surface leading to a possible subclinical tissues inflammation. So that flogosis can be considered as a protective reaction against various noxae. Both innate and adaptive immunity participate to the defensive systems of the ocular surface. Several mechanisms were indicated as promoters for innate immunity. Among these were described the altered production of molecules such as lactoferrin, lysozyme, lipocalin, secretory immunoglobulin A, acidic mammalian chitinase, phospholipase A2, transglutaminase 2, together with the activation of toll-like receptors. Irritating stimuli, such as hyperosmolar tears, determine in the epithelial cells the interaction with receptors that activate response pathways, such as mitogen-activated protein kinases, leading to the production of pro-inflammatory molecules. These events, occurring on both epithelial and dendritic cells, are responsible for the onset and maintaining of inflammation on the ocular surface. Since an overlap of the two forms of DE is often present, it is difficult to differentiate between them. Finding biomarkers that could help this differentiation would be of great relevance for the clinical practice. However, the dynamic evolution of the disease and the peculiar organization of the ocular surface render the identification of a single biomarker of the disease highly unlikely. Much more promising is the effort to identify molecules able to indicate a specific stage of a disease and a possible marker of therapeutic response.

The role of innate immunity in dry eye syndrome

RANIA, Laura;POSTORINO, ELISA IMELDE;PUZZOLO, Domenico;ARAGONA, Pasquale
2013-01-01

Abstract

Dry eye syndrome, (DE), also known as dysfunctional tear syndrome (DTS), is an inflammatory condition of the ocular surface derived by tear hyperosmolarity consequent to either increased tear evaporation (EDE) or aqueous deficiency (ADDE). Several external stimuli continuously trigger the ocular surface leading to a possible subclinical tissues inflammation. So that flogosis can be considered as a protective reaction against various noxae. Both innate and adaptive immunity participate to the defensive systems of the ocular surface. Several mechanisms were indicated as promoters for innate immunity. Among these were described the altered production of molecules such as lactoferrin, lysozyme, lipocalin, secretory immunoglobulin A, acidic mammalian chitinase, phospholipase A2, transglutaminase 2, together with the activation of toll-like receptors. Irritating stimuli, such as hyperosmolar tears, determine in the epithelial cells the interaction with receptors that activate response pathways, such as mitogen-activated protein kinases, leading to the production of pro-inflammatory molecules. These events, occurring on both epithelial and dendritic cells, are responsible for the onset and maintaining of inflammation on the ocular surface. Since an overlap of the two forms of DE is often present, it is difficult to differentiate between them. Finding biomarkers that could help this differentiation would be of great relevance for the clinical practice. However, the dynamic evolution of the disease and the peculiar organization of the ocular surface render the identification of a single biomarker of the disease highly unlikely. Much more promising is the effort to identify molecules able to indicate a specific stage of a disease and a possible marker of therapeutic response.
2013
9781628080384
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/2603773
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