- National Eye Institute, NIH, Postdoctoral Fellow
- University of Pittsburgh School of Medicine, PhD, Immunology
- University of Pittsburgh, BS, Biological Sciences
Education & Training
Commensal-derived Trehalose Monocorynomycolate Triggers γδ T Cell-driven Protective Ocular Barrier Immunity. Xu X, Rigas YE, Mattapallil MJ, Guo J, Nagarajan V, Bohrnsen E, Richards C, Gupta A, Gaud G, Love PE, Jiang T, Zhang A, Xu B, Peng Z, Jittayasothorn Y, Carr M, Magone MT, Brandes NT, Shane J, Schwarz B, St Leger AJ, Caspi RR. bioRxiv [Preprint]. 2025 Mar 18:2025.03.17.643820. doi: 10.1101/2025.03.17.643820.
Immunomodulation by the combination of statin and matrix-bound nanovesicle enhances optic nerve regeneration. Campbell GP, Amin D, Hsieh K, Hussey GS, St Leger AJ, Gross JM, Badylak SF, Kuwajima T. NPJ Regen Med. 2024 Oct 26;9(1):31. doi: 10.1038/s41536-024-00374-y.
Living with your biome: how the bacterial microbiome impacts ocular surface health and disease. Lai J, Rigas Y, Kantor N, Cohen N, Tomlinson A, St Leger AJ, Galor A. Expert Rev Ophthalmol. 2024;19(2):89-103. doi: 10.1080/17469899.2024.2306582. Epub 2024 Feb 4.
The Secreted Ly6/uPAR-Related Protein 1 (Slurp1) Modulates Corneal Angiogenic Inflammation Via NF-κB Signaling. Swamynathan S, Campbell G, Sohnen P, Kaur S, St Leger AJ, Swamynathan SK. Invest Ophthalmol Vis Sci. 2024 Jan 2;65(1):37. doi: 10.1167/iovs.65.1.37.
Genetic Manipulation of Corynebacterium mastitidis to Better Understand the Ocular Microbiome. Rigas Y, Treat BR, Shane J, Shanks RMQ, St Leger AJ. Invest Ophthalmol Vis Sci. 2023 Feb 1;64(2):19. doi: 10.1167/iovs.64.2.19.
We have pioneered research in a historically understudied area of ophthalmology, the ocular microbiome and its effect(s) on ocular disease. Normally a highly contentious topic in ophthalmology, the ocular microbiome does, indeed, tune local immunity to prevent fungal and bacterial infection. Now, the St. Leger lab aims to extend those findings to explore how ocular resident bacteria may modulate immunity against viral infections like herpes simplex virus type 1 (HSV-1), which have the potential cause blindness. To this end, the laboratory uses Corynebacterium masitidis as a candidate colonizer to explore how the ocular immunity is developed and maintained. Further, the lab has a keen interest in understanding mechanisms controlling gd T cells, which are critical for protection of the ocular surface from disease.
Future goals include the development of novel probiotic-like therapies for the treatment of diseases at the ocular surface. In addition, we are interested in how the local microbiome may affect intraocular diseases like glaucoma or age-related macular degeneration where the microbiome has been implicated but not proven for the development and progression of disease.
A separate arm of research in the laboratory focuses on investigating how corneal nerves affect the development of ocular disease. In healthy individuals, the cornea, which is the most densely innervated tissue in the body, is innervated by sensory nerves that control the blink reflex and allow the eye to wash away potential pathogens, allergens, and/or irritants. After infection with HSV-1, corneal sensory nerves retract and are replaced with sympathetic nerves, which lack the ability to sense stimuli. As a result, the infected eye loses the ability to blink, which leaves the ocular surface susceptible to trauma and drying. We hypothesize that this mechanism is largely responsible for the disease associated with HSV-1 infection. Current research in the lab focuses on identifying specific factors regulating sensory nerve retraction and sympathetic nerve growth in hopes of developing novel therapies that preserve blink reflexes.
National Eye Institute