Boston, Mass. - Scientists at Schepens Eye Research Institute have found that an inflammatory immune response, which is suppressed in the normal eye, may be an early, perhaps the first, step in the onset of a kind of glaucoma known as pigment dispersion glaucoma. They also found that replacing the inflammation-causing immune cells in the bone marrow with normal donor cells restored the eye's "immune privileged state, inhibited inflammation in the eye, and ultimately prevented the glaucoma. These findings, published in the current issue of the Journal of Experimental Medicine (May 19, 2003), are the first evidence of a direct link between abnormal inflammatory immune responses and any type of glaucoma, and may ultimately point to novel treatments for this and other types of glaucoma.
"This is just the tip of the iceberg", says J. Wayne Streilein, MD, senior scientist at Schepens Eye Research Institute and senior author of the study. "We have long suspected 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".
According to Streilein, the team chose to study this particular type of glaucoma because there was a mouse model available. A strain of mice with pigment dispersion glaucoma had been discovered five years ago by Dr. Simon John of the Jackson Laboratories in Maine, who also was able to identify two mutant genes connected with the disease. "Although we knew the genes, because of Dr. John's seminal work, we still did not know the chain of events they caused," said Streilein. "So we decided to explore whether these mice, whose progression toward pigment dispersion glaucoma was similar (although more rapid and intense) to that in humans, had abnormal immune responses in their eyes", says Streilein.
Glaucoma is the second leading cause of b
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Contact: Patti Jacobs
pattijacobs@hotmail.com
617-912-2544
Schepens Eye Research Institute
28-May-2003
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