Abstract
Presentation Description :
It is well recognized that ocular surface inflammation plays a prominent role in dry eye disease (DED) symptom development and amplification. Our laboratory has discovered that numerous neutrophils are present on the ocular surface of patients with severe tear-deficient DED subtypes and that they release their nuclear chromatin complex as a type of biologic “spider’s web”. These extracellular DNA (eDNA) webs are termed neutrophil extracellular traps (NETs). Although NETs are part of the innate immune defense, they may contribute to pathology of chronic inflammatory diseases like rheumatoid arthritis and systemic lupus erythematosus. We showed that in severe tear-deficient DED patients, including chronic ocular graft-vs.-hostdisease (oGVHD) patients, there were excessive amounts of extracellular DNA (eDNA) and molecular components of neutrophil extracellular traps (NETs) over the ocular surface. NETs accumulate on the ocular surface of oGVHD patients either because of increased formation (due to hyperosmolarity) and/or reduced clearance (due to tear deficiency and consequent nuclease deficiency). In this presentation, we will describe the diagnostic and therapeutic implications of NETs in Chronic Ocular GVHD.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.