The etiology of dry eye disease (DED) is complex and not yet fully understood, but the disease is now recognized as being associated with ocular surface inflammation. The latest advances in the understanding of the pathophysiology of DED have directed the focus of recent drug development to target the inflammatory pathways involved in the disease. Lifitegrast is a novel small molecule integrin antagonist that inhibits T cell-mediated inflammation by blocking the binding of two important cell surface proteins (lymphocyte function-associated antigen 1 and intercellular adhesion molecule 1), thus lessening overall inflammatory responses. This review highlights the role of T cells and integrins in the inflammatory process involved in the pathophysiology of DED and outlines the scientific rationale for the role of lifitegrast. In addition, the preclinical development, pharmacological properties, clinical efficacy, and safety of lifitegrast are described.

Azithromycin provided significant improvement in signs and symptoms of blepharitis after 4 weeks of treatment compared with baseline and persisted in the 4-week follow-up period.