During most eye infections or injuries, neutrophils, immune cells found in the blood, are usually the first line of defense. However, National Eye Institute research at the Flaum Eye Institute and Del Monte Institute for Neuroscience at the University of Rochester have discovered that the retina responds differently than many other tissues in the body. When photoreceptor cells in the retina are damaged, microglia, or the brain’s immune cells, respond, and the neutrophils are not recruited to help despite passing through nearby blood vessels.
“This finding has high implications for what happens for millions of Americans who suffer vision loss through loss of photoreceptors,” said Jesse Schallek, Ph.D., associate professor of ophthalmology and senior author of a study published in eLife.
“This association between two key immune cell populations is essential knowledge as we build new therapies that must understand the nuance of immune cell interactions,” Schallek said.
Using adaptive optics imaging, a camera technology developed by the University of Rochester that allows the imaging of single neurons and immune cells inside the living eye, researchers studied the retinas of mice with photoreceptor damage. They found that while both neutrophil and microglia cells are present in the retina, only microglia cells respond to photoreceptor injury, and they do not call upon neutrophils to help repair the photoreceptor damage. Researchers believe this suggests a type of cloaking occurs during retinal injury to protect the retina from a rush of immune cells that could do more harm than good.
“What is remarkable here is that the passing neutrophils are so close to the reactive microglia, and yet they do not signal to them to assist in damage recovery,” said Schallek.
“This is notably different than what is seen in other areas of the body where neutrophils are the first to respond to local damage and mount an early and robust response.”
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