Inflammatory immune response may be first step in pigment dispersion glaucoma

An inflammatory immune response may be an early step in the onset of pigment dispersion glaucoma, researchers at Boston’s Schepens Eye Research Institute suggest. By replacing inflammation-causing immune cells in the bone marrow in a mouse model with normal donor cells, the inflammation in the eye was inhibited, and this ultimately prevented the onset of this form of glaucoma, the researchers said.

J. Wayne Streilein, MD, noted that there has been suspicion that “an inappropriate immune response or loss of ‘immune privilege’ in the eye may be a precursor or the first trigger that sets certain blinding eye diseases on their inevitable course of destruction. This is the first formal evidence to support this theory.”

In the mouse model of pigment dispersion syndrome, melanin is shed into the anterior portion of the eye. As in humans, the resulting increased intraocular pressure strangles the optic nerve and kills retinal cells. In this study, the researchers examined the mouse eyes before visible onset of the disease to determine if the eyes suppressed T-cell activation, which they did. By replacing the bone marrow of mice destined to develop the disease, the immune-privileged status was maintained in the eyes, inflammation never developed and pigment dispersion failed to occur.

The results are published in the Journal of Experimental Medicine.