gms | German Medical Science

102. Jahrestagung der DOG

Deutsche Ophthalmologische Gesellschaft e. V.

23. bis 26.09.2004, Berlin

Immune amplification in inflammatory corneal neovascularization

Meeting Abstract

Search Medline for

  • corresponding author C. Cursiefen - Augenklinik mit Poliklinik, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen

Evidenzbasierte Medizin - Anspruch und Wirklichkeit. 102. Jahrestagung der Deutschen Ophthalmologischen Gesellschaft. Berlin, 23.-26.09.2004. Düsseldorf, Köln: German Medical Science; 2004. Doc04dogDO.11.08

The electronic version of this article is the complete one and can be found online at:

Published: September 22, 2004

© 2004 Cursiefen.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.




Corneal hemangiogenesis (CHA) and corneal lymphangiogenesis (CLA) are associated with inflammatory diseases of the cornea. Aim of this study was to unravel the precise role of inflammatory cells, and especially macrophages, in inducing pathologic corneal neovascularization.


The effect of systemic depletion of bone marrow derived-cells (by irradiation) and local depletion of macrophages (using clodronate liposomes) on inflammation-induced CHA and CLA was analyzed using the mouse model of suture-induced neovascularization. The extent of CHA and CLA was quantified by morphometry of CD31/LYVE-1 stained corneal flatmounts.


Both systemic as well as local depletion of bone marrow-derived cells and specifically macrophages nearly completely inhibited CHA and CLA. Furthermore, inhibition of macrophage recruitment via VEGF-A/VEGFR1 using a molecular trap for VEGF-A (VEGF TrapR1R2) had the same effect.


VEGF-A mediated recruitment of bone marrow derived macrophages seems to be an essential early step in immune-amplification leading to both pathological corneal hem- and lymphangiogenesis. Targeting of macrophages opens new avenues for inhibiting pathologic hem- and lymphangiogenesis.

Support: DFG (Cu 47/1-1, Cu 47/1-2), IZKF Erlangen, NIH (EY10765)