Journal
ANGIOGENESIS
Volume 22, Issue 2, Pages 311-323Publisher
SPRINGER
DOI: 10.1007/s10456-018-9658-x
Keywords
Inflammation; Angiogenesis; Tumor; Cytokine
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Funding
- NEI NIH HHS [K08 EY028999] Funding Source: Medline
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T(H)17 cells play important yet complex roles in cancer development and progression. We previously reported that T(H)17 cells and IL-17 mediate resistance to anti-VEGF therapy by inducing recruitment of immunosuppressive and proangiogenic myeloid cells to the tumor microenvironment. Here, we demonstrate that IL-22, a key effector cytokine expressed by T(H)17 cells, directly acts on endothelial cells to promote tumor angiogenesis. IL-22 induces endothelial cell proliferation, survival, and chemotaxis in vitro and neovascularization in an ex vivo mouse choroid explant model. Blockade of IL-22, with a neutralizing antibody, significantly inhibits tumor growth associated with reduced microvascular density. No synergistic effect of IL-22 with VEGF was observed. These results identify IL-22 as a potential therapeutic target for blocking tumor angiogenesis.
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