"CCR3 chemokine receptor is known to be a key player in the allergic inflammation process, but Dr. Ambati's studies have now identified CCR3 as a key marker of the CNV process involved in AMD. If researchers can determine why CCR3 is expressed in the CNV of AMD patients, they could further understand AMD disease progression," said Dr. Grace L. Shen, director of the ocular immunology and inflammation program at the National Eye Institute.
Ambati's research team was able to detect these same abnormal blood vessels in the living eyes of mice by attaching anti-CCR3 antibodies to tiny semiconductor nanocrystals called "quantum dots" and injecting these into the mice. The antibodies cause the quantum dots to attach to CCR3 on the surface of the abnormal blood vessels, making them visible with conventional ocular angiography techniques, even before they have penetrated the retina. This was not possible before.
"This is an exciting discovery for the millions of people at risk of developing wet macular degeneration, because this new imaging technology introduces the possibility of detecting pathological neovascularization before retinal damage and vision loss occur," said Dr. Stephen J. Ryan, professor of ophthalmology at the University of Southern California and member of the National Academy of Sciences' Institute of Medicine.
The research team discovered that CCR3 not only provides a unique signature for CNV, but the gene actively promotes the growth of these abnormal blood vessels in the eye. Thus the same anti-CCR3 antibodies used to detect CNV could potentially be useful as a clinical treatment to prevent macular degeneration.
The early results look promising. Treatment with anti-CCR3 antibodies reduced CNV in mice by about 70 percent, as opposed to 60 percent with VEGF-based treatments currently in clinical use. Ambati says Phase I clinical trials are not far off.
"The identification of CCR3 on the endothelial cells
|Contact: Keith Hautala|
University of Kentucky