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Mediators Inflamm. 2018 Aug 12;2018:2532314. doi: 10.1155/2018/2532314. eCollection 2018.

Innate and Adaptive Cell Populations Driving Inflammation in Dry Eye Disease.

Author information

1
Universidad Nacional Autónoma de México (UNAM), Laboratorio de Inmunología experimental y Regulación de la inflamación Hepato-Intestinal, UBIMED, Facultad de Estudios Superiores (FES) Iztacala, Tlalnepantla, MEX, Mexico.
2
University of Calgary, Snyder Institute for Chronic Diseases, Cumming School of Medicine, Calgary, AB, Canada.
3
Aspen Woods Clinic, Calgary, AB, Canada.
4
Universidad Nacional Autónoma de México (UNAM), Unidad de Biomedicina (UBIMED), Facultad de Estudios Superiores (FES) Iztacala, Tlalnepantla, MEX, Mexico.
5
Universidad Nacional Autónoma de México (UNAM), Laboratorio de Enfermedades Inflamatorias Oculares, Carrera de Optometría, Facultad de Estudios Superiores (FES) Iztacala, Tlalnepantla, MEX, Mexico.

Abstract

Dry eye disease (DED) is the most common ocular disease and affects millions of individuals worldwide. DED encompasses a heterogeneous group of diseases that can be generally divided into two forms including aqueous-deficient and evaporative DED. Evidence suggests that these conditions arise from either failure of lacrimal gland secretion or low tear film quality. In its secondary form, DED is often associated with autoimmune diseases such as Sjögren's syndrome and rheumatoid arthritis. Current treatment strategies for DED are limited to anti-inflammatory medications that target the immune system as the source of deleterious inflammation and tissue injury. However, there is a lack of understanding of the underlying pathogenesis of DED, and subsequently, there are very few effective treatment strategies. The gap in our knowledge of the etiology of primary DED is in part because the majority of research in DED focused on secondary autoimmune causes. This review focuses on what is currently understood about the contribution of innate and adaptive immune cell populations in the pathogenesis of DED and highlights the need to continue investigating the central role of immunity driving DED.

PMID:
30158831
PMCID:
PMC6109495
DOI:
10.1155/2018/2532314
[Indexed for MEDLINE]
Free PMC Article

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