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Cancer Research 69, 2010, March 1, 2009. Published Online First February 24, 2009;
doi: 10.1158/0008-5472.CAN-08-3479
© 2009 American Association for Cancer Research
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Immunology

IFN{gamma} Promotes Papilloma Development by Up-regulating Th17-Associated Inflammation

Mingjie Xiao1,2,3, Chunhui Wang1,2,3, Jinhua Zhang1,2, Zhiguang Li1,2,3, Xueqiang Zhao1,2,3 and Zhihai Qin1,2

1 National Laboratory of Biomacromolecules, 2 Chinese Academy of Sciences-University of Tokyo Joint Laboratory of Structural Virology and Immunology, and 3 Graduate School of the Chinese Academy of Sciences, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China

Requests for reprints: Zhihai Qin, Institute of Biophysics, Chinese Academy of Sciences, 15 Datun Road, Beijing 100101, China. Phone: 86-10-64888435; Fax: 86-10-64848257; E-mail: zhihai{at}ibp.ac.cn.

Key Words: IFN{gamma} • Skin carcinogenesis • Papilloma • Th17 • Inflammation

IFN{gamma} plays a crucial role in immunity against a variety of transplanted tumors and methylcholanthrene-mediated tumorigenesis in mice. However, it is not clear whether and how endogenous IFN{gamma} influences 7,12-dimethylbenz(a)anthracene (DMBA)–induced and 12-O-tetradecanoylphorbol-13-acetate (TPA)–induced papilloma development. We found here that IFN{gamma} expression was markedly up-regulated shortly after DMBA/TPA application to the skin. Surprisingly, neutralizing IFN{gamma} activity in vivo did not increase but rather decreased tumor development. Furthermore, IFN{gamma} receptor–deficient mice were also more resistant to papilloma development than their counterparts were. IFN{gamma} acted mainly in the promotion stage of papilloma development by enhancing TPA-induced leukocyte infiltration and epidermal hyperproliferation. The up-regulation of tumor necrosis factor {alpha}, interleukin (IL)-6, and transforming growth factor β was largely dependent on host IFN{gamma} responsiveness. Remarkably, up-regulation of both IL-17 expression in the skin and T helper 17 (Th17) cell number in draining lymph nodes after DMBA/TPA treatment was dependent on IFN{gamma} signaling. Depletion of IL-17 not only decreased the DMBA/TPA–induced inflammation and keratinocyte proliferation but also delayed papilloma development. These results show that IFN{gamma}, under certain conditions, may promote tumor development by enhancing a Th17-associated inflammatory reaction. [Cancer Res 2009;69(5):2010–7]




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L. Wang, T. Yi, M. Kortylewski, D. M. Pardoll, D. Zeng, and H. Yu
IL-17 can promote tumor growth through an IL-6-Stat3 signaling pathway
J. Exp. Med., July 6, 2009; 206(7): 1457 - 1464.
[Abstract] [Full Text] [PDF]


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Copyright © 2009 by the American Association for Cancer Research.