| First Author | Hasegawa E | Year | 2013 |
| Journal | J Immunol | Volume | 190 |
| Issue | 4 | Pages | 1778-87 |
| PubMed ID | 23319736 | Mgi Jnum | J:193317 |
| Mgi Id | MGI:5468183 | Doi | 10.4049/jimmunol.1202495 |
| Citation | Hasegawa E, et al. (2013) IL-23-Independent Induction of IL-17 from gammadeltaT Cells and Innate Lymphoid Cells Promotes Experimental Intraocular Neovascularization. J Immunol 190(4):1778-87 |
| abstractText | Choroidal neovascularization (CNV) is a characteristic of age-related macular degeneration. Genome-wide association studies have provided evidence that the immune system is involved in the pathogenesis of age-related macular degeneration; however, the role of inflammatory cytokines in CNV has not been established. In this study, we demonstrated that IL-17 had a strong potential for promoting neovascularization in a vascular endothelial growth factor-independent manner in laser-induced experimental CNV in mice. Infiltrated gammadeltaT cells and Thy-1(+) innate lymphoid cells, but not Th17 cells, were the main sources of IL-17 in injured eyes. IL-23 was dispensable for IL-17 induction in the eye. Instead, we found that IL-1beta and high-mobility group box 1 strongly promoted IL-17 expression by gammadeltaT cells. Suppression of IL-1beta and high-mobility group box 1, as well as depletion of gammadeltaT cells, reduced IL-17 levels and ameliorated experimental CNV. Our findings suggest the existence of a novel inflammatory cytokine network that promotes neovascularization in the eye. |
