IOVS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

(Investigative Ophthalmology and Visual Science. 2008;49:2143-2147.)
© 2008 by The Association for Research in Vision and Ophthalmology, Inc.
doi:10.1167/iovs.07-0523
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Takahashi, H.
Right arrow Articles by Yanagi, Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Takahashi, H.
Right arrow Articles by Yanagi, Y.

Suppression of Choroidal Neovascularization by Vaccination with Epitope Peptide Derived from Human VEGF Receptor 2 in an Animal Model

Hidenori Takahashi,1 Hidenobu Ishizaki,2 Hideaki Tahara,2 Yasuhiro Tamaki,*,1 and Yasuo Yanagi*,1

1From the Department of Ophthalmology and the 2Department of Surgery and Bioengineering, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.

PURPOSE. It has been shown that vaccination with peptides derived from human vascular endothelial growth factor receptor 2 (VEGFR2) induces cytotoxic T lymphocytes (CTLs) with potent cytotoxicity against endothelial cells expressing VEGFR2 in a A2/Kb transgenic mice system expressing human HLA-A*0201. The present study examined the efficacy of this immunotherapy against age-related macular degeneration (AMD) using a choroidal neovascularization (CNV) model.

METHODS. Seven- to 10-week-old A2/Kb transgenic mice expressing human HLA-A*0201 were used. The mice were divided into three groups of 15 animals each: phosphate-buffered saline (PBS) treatment (control); immunity adjuvant (incomplete Freund adjuvant [IFA]); and antigen peptide of human VEGFR 2 and IFA (peptide vaccination group). Immunization was given on days 0 and 11. On day 20, six CNVs were induced in both eyes of each animal using a semiconductor laser set to 75 µm, 200 mW, and 0.05 seconds. Leakage from the CNV was measured by fluorescein angiography 7 days after laser treatment. CNV volume was measured using a choroidal flatmount after perfusing the mice with fluorescein conjugate lectin.

RESULTS. There were no significant differences in the leakage or the area of CNV in the IFA-treated group compared with controls. In contrast, the fluorescent leakage index in the peptide vaccination group was reduced to 80% and the CNV area to 18% compared with the control group (P < 0.0001 and P < 0.05, respectively).

CONCLUSIONS. This model provides a rationale for immunotherapy using the epitope peptides derived from VEGFR2 for the treatment of CNV.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2008 by the Association for Research in Vision and Ophthalmology