IL-23-independent induction of IL-17 from γδT cells and innate lymphoid cells promotes experimental intraocular neovascularization

Eiichi Hasegawa, Koh Hei Sonoda, Takashi Shichita, Rimpei Morita, Takashi Sekiya, Akihiro Kimura, Yuji Oshima, Atsunobu Takeda, Takeru Yoshimura, Shigeo Yoshida, Tatsuro Ishibashi, Akihiko Yoshimura

研究成果: Contribution to journalArticle査読

59 被引用数 (Scopus)

抄録

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 γδT 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-1β and high-mobility group box 1 strongly promoted IL-17 expression by γδT cells. Suppression of IL-1β and high-mobility group box 1, as well as depletion of γδT 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.

本文言語英語
ページ(範囲)1778-1787
ページ数10
ジャーナルJournal of Immunology
190
4
DOI
出版ステータス出版済み - 2 15 2013

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

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