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M. J. McConnell, J. Z. Baffi, H. Kaneko, J. C. Pate, M. E. Kleinman, S. Dridi, R. J. C. Albuquerque, P. Pearson, J. Ambati; CCR3 as a Candidate Target for Presumed Ocular Histoplasmosis Syndrome Diagnosis and Therapy. Invest. Ophthalmol. Vis. Sci. 2010;51(13):3351.
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Recently we identified CCR3 as a new marker of pathological angiogenesis and as a functional target in neovascular age-related macular degeneration (AMD). The goal of this study is to examine whether choroidal neovascular vessels (CNV) in presumed ocular histoplasmosis syndrome (POHS) also express CCR3. We also studied whether vascular hyperpermeability, a feature of CNV in POHS, was sensitive to CCR3 inhibition.
Fibrovascular complexes from patients with POHS were excised by subretinal surgery. The excised subretinal membranes were comprehensively analyzed using histopathology and immunohistochemistry for CCR3 and endothelial cells (CD31). Fluorescein angiography was performed in mice treated with neutralizing anti-CCR3 antibodies versus isotype IgG following laser injury-induced CNV.
In all (6/6) fibrovascular membranes, CD31 positive endothelial cells expressed CCR3 immunoreactivity. CCR3 neutralization dramatically reduced CNV leakage in the mouse model.
These data suggest that CCR3 targeting may be a viable strategy for the early detection and treatment of choroidal neovascularization in the setting of POHS.
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