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CL1R2 antibody, as well as Bevacizumab, promotes the regression of pathologic retinal neovascularisation in Vldlr knockout mice
Author(s) -
SOLER V,
HAMID S,
TOLOU C,
TRICOIRE C,
DAUSSION MA,
LE BOUTEILLER P,
CASSAGNE M,
CALVAS P,
MALECAZE F,
GALIACY S
Publication year - 2014
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2014.4743.x
Subject(s) - medicine , macular degeneration , bevacizumab , retinal , choroidal neovascularization , neovascularization , monoclonal antibody , knockout mouse , ophthalmology , pathology , antibody , immunology , angiogenesis , receptor , chemotherapy
Purpose Very low‐density lipoprotein receptor mutant mice (Vldlr(‐/‐)) demonstrate retinal neovascularisation. Monoclonal antibody CL1‐R2 recognizes human membrane receptor CD160, which is expressed on activated endothelial cells of neovessels but not in vessels of healthy tissues. In this study, we evaluated the therapeutic potential of CL1R2 antibody in Vldlr(‐/‐) mice as a model for exudative age‐related macular degeneration and macular telangiectasia. Methods Thirty Vldlr(‐/‐) mice benefitted at postnatal day (P) 42 from retinal angiography. Mice population was then divided in three groups (ten mice per group). According to the groups, mice underwent intravitreal injection of CL1‐R2 or Bevacizumab or control antibody. At P56, mice benefitted from angiography and were sacrificed. Results At P42, Vldlr(‐/‐) retinas presented with neovascular lesions. At P56, we observed decrease of neovascular lesions in eyes treated with CL1R2 antibody and with bevacizumab. This decrease of neovascular lesions was not observed in control mice. Conclusion CL1R2 antibody, as well as Bevacizumab, promotes the regression of pathologic retinal neovascularization in the Vldlr knockout mouse. As CL1R2 is an activator of NK cells, our result suggest that the activation of NK cells inhibits the development of Vldlr(‐/‐) mice retinal neovascularisation.