IL-27 inhibits pathophysiological intraocular neovascularization due to laser burn

Eiichi Hasegawa, Yuji Oshima, Atsunobu Takeda, Kazuko Saeki, Hiroki Yoshida, Koh Hei Sonoda, Tatsuro Ishibashi

Research output: Contribution to journalArticlepeer-review

18 Citations (Scopus)

Abstract

AMD is the most common disease leading to acquired blindness in developed countries. CNV is the foremost cause of AMD and is thought to be induced by regional inflammation as a result of age-related conformational changes of the chorioretinal interface. Here, we show that IL-27, a member of the IL-6/IL-12 cytokine family, has an angiostatic effect and regulates the development of laser-induced experimental CNV in mice. In this model, IL-27 expression increased in the damaged choroid and peaked at the 24 h-time-point. IL-27 neutralization, induced by inoculating an antagonistic antibody into the vitreous cavity, enhanced VEGF production and the extent of CNV. By contrast, the administration of rIL-27 reduced VEGF production and the extent of CNV. Mice deficient in the EBI3, which lack IL-27, also showed more CNV than C57BL/6 mice, and this was reduced by IL-27 supplementation. We additionally investigated the effect of IL-27 on the function of mac-rophages, which play a critical role in CNV. IL-27 did not affect macrophage migration but inhibited its VEGF production. IL-27 therefore appears to regulate CNV and is a promising candidate target for treating sight-threatening diseases caused by ocular neovascularization.

Original languageEnglish
Pages (from-to)267-273
Number of pages7
JournalJournal of Leukocyte Biology
Volume91
Issue number2
DOIs
Publication statusPublished - Feb 2012

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Cell Biology

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