Replacing Immune Cells May Impede Onset of Glaucoma
A study in the Journal of Experimental Medicine (2003;197:1335-1344) found that inflammatory immune response, which is suppressed in the normal eye, might be an early step in the onset of pigment dispersion glaucoma. Pigment dispersion glaucoma occurs when the iris begins to shed melanin into the front part of the eye. This is followed by increasing pressure within the eye, which strangles the optic nerve and kills the retinal cells attached to it.
The researchers examined the eyes of model mice with pigment dispersion glaucoma before the visible onset of the disease and found that the diseased eyes failed to successfully suppress T-cells--white blood cells that cause the iris to shed pigment. This failure preceded clinical evidence of pigment dispersion. They also found that the eyes contained bone marrow-derived white blood cells that were programmed to cause inflammatory responses. Jun Song Mo, M.D., the study's lead author, told the press, "It is relevant that one of the two genes known to be responsible for pigment dispersion glaucoma in mice is active in these same white blood cells."
The research team concluded that the eyes of the genetically predisposed mice lost immune privilege before the pigment dispersion began.
"What this suggested to us," said J. Wayne Streilein, M.D., senior author of the study, "is that maybe the first thing that the genes for pigment dispersion glaucoma do is break down immune privilege and leave the eyes vulnerable to inflammation."
The researchers tested their theory of inappropriate immune response even further by replacing the bone marrow of mice predetermined to develop pigment dispersion glaucoma with bone marrow from normal mice. Following the procedure, the team found that the immune-privileged status was maintained in the eyes, inflammation never developed and pigment dispersion failed to occur.
"These results are very exciting and encouraging. We feel that this is a major breakthrough in understanding how this disease is triggered and may be cured," said Streilein. "We are eager to understand more completely the interrelationship between loss of immune privilege and development of glaucoma. Moreover, we are also interested to know whether a similar immune dependency might occur in other blinding eye diseases, such as macular degeneration and retinitis pigmentosa"--AR