In his second lecture, Gadek reviews the molecular mechanism of dry eye syndrome, focusing on the role of inflammation and T-cells in this disorder.  By analyzing clinical trial data from other drugs developed to treat dry eye, Gadek and colleagues confirmed the importance of LFA-1 as a possible target.  LFA-1 is a surface protein on T-cells that binds to ICAM-1 on antigen presenting cells, T-cells,  and epithelial cells and causes inflammation.  Gadek and his colleagues developed Lifitegrast, a small molecule that serves as an ICAM-1 mimetic. By binding to LFA-1 on T-cells, Lifitegrast inhibits the binding of ICAM-1 and therefore inhibits the inflammation associated with dry eye syndrome.