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Wang, Zhen; Zeng, Fan-Lian; Hu, Ya-Wen; Wang, Xiao-Yan; Zhao, Fu-Lei; Zhou, Pei; Hu, Jing; Xiao, Yuan-Yuan; Hu, Zhong-Lan; Guo, Ming-Feng; Wei, Xiao-Qiong; Liu, Xiao; Huang, Nong-Yu; Zhang, Jun; Chen, Shu-Wen; Cheng, Juan; Zheng, Hua-Ping; Zhou, Hong; Zhao, Qi-Xiang; Zhang, Chen; Hao, Yan; Zou, Song; Gui, Yi-Yue; Yu, Jia-Dong; Gu, Lin-Na; Yue, Cheng-Cheng; Zhang, Hao-Zhou; Wu, Wen-Ling; Zhou, Yi-Fan; Zhou, Xi-Kun; Shen, Guo-Bo; Teng, Xiu; Li, Jiong
Signal transduction and targeted therapy, 01/2022, Volume: 7, Issue: 1Journal Article
Interleukin-37b (hereafter called IL-37) was identified as fundamental inhibitor of natural and acquired immunity. The molecular mechanism and function of IL-37 in colorectal cancer (CRC) has been elusive. Here, we found that IL-37 transgenic (IL-37tg) mice were highly susceptible to colitis-associated colorectal cancer (CAC) and suffered from dramatically increased tumor burdens in colon. Nevertheless, IL-37 is dispensable for intestinal mutagenesis, and CRC cell proliferation, apoptosis, and migration. Notably, IL-37 dampened protective cytotoxic T cell-mediated immunity in CAC and B16-OVA models. CD8 T cell dysfunction is defined by reduced retention and activation as well as failure to proliferate and produce cytotoxic cytokines in IL-37tg mice, enabling tumor evasion of immune surveillance. The dysfunction led by IL-37 antagonizes IL-18-induced proliferation and effector function of CD8 T cells, which was dependent on SIGIRR (single immunoglobulin interleukin-1 receptor-related protein). Finally, we observed that IL-37 levels were significantly increased in CRC patients, and positively correlated with serum CRC biomarker CEA levels, but negatively correlated with the CD8 T cell infiltration in CRC patients. Our findings highlight the role of IL-37 in harnessing antitumor immunity by inactivation of cytotoxic T cells and establish a new defined inhibitory factor IL-37/SIGIRR in cancer-immunity cycle as therapeutic targets in CRC.
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