US Patent Number
8778616
Publication Date
7-15-2014
Abstract
The results presented herein demonstrate the specific expression of CCR3 in CNV endothelial cells in humans with AMD, and despite the expression of its ligands, eotaxin-1, -2, and -3, neither eosinophils nor mast cells are present in human CNV. The genetic or pharmacological targeting of CCR3 or eotaxins as disclosed herein inhibited injury-induced CNV in mice. CNV suppression by CCR3 blockade was due to direct inhibition of endothelial cell proliferation, and was uncoupled from inflammation as it occurred in mice lacking eosinophils or mast cells and was independent of macrophage and neutrophil recruitment. CCR3 blockade was more effective at reducing CNV than vascular endothelial growth factor-A (VEGF-A) neutralization, which is currently in clinical use, and, unlike VEGF-A blockade, not toxic to the mouse retina. In vivo imaging with CCR3-targeting quantum dots located spontaneous CNV invisible to standard fluorescein angiography in mice before retinal invasion. CCR3 targeting is useful in reducing vision loss due to AMD through early detection and therapeutic angioinhibition.
Assignees
University of Kentucky Research Foundation, Lexington, KY (US)
Application Number
13/322,087
Filing Date
05/26/2010
Recommended Citation
Ambati, Jayakrishna and Kleinman, Mark E., "Method of Using CCR3 Binding Agents to Detect Choroidal Neovascularization" (2014). Ophthalmology and Visual Science Faculty Patents. 5.
https://uknowledge.uky.edu/ophthalmology_patents/5
