Abstract
Injuries to the cornea can lead to recurrent corneal erosions, compromising its barrier function and increasing the risk of infection. Vital as corneal integrity is to the eye's optical power and homeostasis, the immune response to corneal erosions remains poorly understood. It is also unknown whether there is coordinated immune activation between the cornea and other regions of the anterior segment to protect against microbial invasion and limit the spread of inflammation when corneal erosions occur. Herein, a corneal debridement wounding model was used to characterize the immune cell phenotypes populating the cornea in response to erosion formation, and whether and which immune cells are concurrently recruited to the surface of the lens was investigated. The formation of corneal erosions induced an influx of myeloid lineage phenotypes, both M2 macrophages associated with tissue healing and wound repair, and Ly6G+ Ly6C+ myeloperoxidase+ cells resembling neutrophils/polymorphonuclear-myeloid-derived suppressor cells (PMN-MDSCs), with few regulatory T cells, into the corneal stroma under erosion sites. This leukocyte migration into the cornea when erosions develop was paralleled by the recruitment of immune cells, predominantly neutrophils/PMN-MDSCs, to the anterior, cornea-facing lens capsule. Both cornea-infiltrating and lens capsule-associated neutrophil/PMN-MDSC-like immune cells produce the anti-inflammatory cytokine IL-10. These findings suggest a collaborative role for the lens capsule-associated immune cells in preventing infections, controlling inflammation, and maintaining homeostasis of the anterior segment during recurrent corneal erosions.