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Dry eye syndrome: developments and lifitegrast in perspective

Authors Lollett IV, Galor A

Received 13 September 2017

Accepted for publication 23 December 2017

Published 15 January 2018 Volume 2018:12 Pages 125—139

DOI https://doi.org/10.2147/OPTH.S126668

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Colin Mak

Peer reviewer comments 2

Editor who approved publication: Dr Scott Fraser


Ivonne V Lollett,1 Anat Galor2,3

1University of Miami, Miller School of Medicine, Miami, FL, 2Ophthalmology Department, Miami Veterans Administration Medical Center, Miami, FL, 3Bascom Palmer Eye Institute, University of Miami, Miller School of Medicine, Miami, FL, USA

Abstract: Dry eye (DE) is a chronic ocular condition with high prevalence and morbidity. It has a complex pathophysiology and is multifactorial in nature. Chronic ocular surface inflammation has emerged as a key component of DE that is capable of perpetuating ocular surface damage and leading to symptoms of ocular pain, discomfort, and visual phenomena. It begins with stress to the ocular surface leading to the production of proinflammatory mediators that induce maturation of resident antigen-presenting cells which then migrate to the lymph nodes to activate CD4 T cells. The specific antigen(s) targeted by these pathogenic CD4+ T cells remains unknown. Two emerging theories include self-antigens by autoreactive CD4 T cells or harmless exogenous antigens in the setting of mucosal immunotolerance loss. These CD4 T cells migrate to the ocular surface causing additional inflammation and damage. Lifitegrast is the second topical anti-inflammatory agent to be approved by the US Food and Drug Administration for the treatment of DE and the first to show improvement in DE symptoms. Lifitegrast works by blocking the interaction between intercellular adhesion molecule-1 and lymphocyte functional associated antigen-1, which has been shown to be critical for the migration of antigen-presenting cells to the lymph nodes as well as CD4+ T cell activation and migration to the ocular surface. In four large multicenter, randomized controlled trials, lifitegrast has proven to be effective in controlling both the signs and symptoms of DE with minimal side effects. Further research should include comparative and combination studies with other anti-inflammatory therapies used for DE.

Keywords: lifitegrast, SAR1118, dry eye syndrome, inflammation, intercellular adhesion molecule 1, lymphocyte function-associated antigen 1

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