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Lack of interleukin-6 in the tumor microenvironment augments type-1 immunity and increases the efficacy of cancer immunotherapy

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/67656

Title: Lack of interleukin-6 in the tumor microenvironment augments type-1 immunity and increases the efficacy of cancer immunotherapy
Authors: Ohno, Yosuke Browse this author
Toyoshima, Yujiro Browse this author
Yurino, Hideaki Browse this author
Monma, Norikazu Browse this author
Xiang, Huihui Browse this author
Sumida, Kentaro Browse this author
Kaneumi, Shun Browse this author
Terada, Satoshi Browse this author
Hashimoto, Shinichi Browse this author
Ikeo, Kazuho Browse this author
Homma, Shigenori Browse this author →KAKEN DB
Kawamura, Hideki Browse this author →KAKEN DB
Takahashi, Norihiko Browse this author
Taketomi, Akinobu Browse this author →KAKEN DB
Kitamura, Hidemitsu Browse this author →KAKEN DB
Keywords: Cytotoxic T cells
dendritic cells
interferon-γ
interleukin-6
programmed death-ligand 1
Issue Date: Oct-2017
Publisher: John Wiley & Sons
Journal Title: Cancer science
Volume: 108
Issue: 10
Start Page: 1959
End Page: 1966
Publisher DOI: 10.1111/cas.13330
Abstract: Conquering immunosuppression in tumor microenvironments is crucial for effective cancer immunotherapy. It is well known that interleukin (IL)-6, a pleiotropic cytokine, is produced in the tumor-bearing state. In the present study, we investigated the precise effects of IL-6 on antitumor immunity and the subsequent tumorigenesis in tumor-bearing hosts. CT26 cells, a murine colon cancer cell line, were intradermally injected into wild-type and IL-6-deficient mice. As a result, we found that tumor growth was decreased significantly in IL-6-deficient mice compared with wild-type mice and the reduction was abrogated by depletion of CD8+ T cells. We further evaluated the immune status of tumor microenvironments and confirmed that mature dendritic cells, helper T cells and cytotoxic T cells were highly accumulated in tumor sites under the IL-6-deficient condition. In addition, higher numbers of interferon (IFN)-γ-producing T cells were present in the tumor tissues of IL-6-deficient mice compared with wild-type mice. Surface expression levels of programmed death-ligand 1 (PD-L1) and MHC class I on CT26 cells were enhanced under the IL-6-deficient condition in vivo and by IFN-γ stimulation in vitro. Finally, we confirmed that in vivo injection of an anti-PD-L1 antibody or a Toll-like receptor 3 ligand, polyinosinic-polycytidylic acid, effectively inhibited tumorigenesis under the IL-6-deficient condition. Based on these findings, we speculate that a lack of IL-6 produced in tumor-bearing host augments induction of antitumor effector T cells and inhibits tumorigenesis in vivo, suggesting that IL-6 signaling may be a promising target for the development of effective cancer immunotherapies.
Rights: http://creativecommons.org/licenses/by-nc/4.0/
Type: article
URI: http://hdl.handle.net/2115/67656
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 北村 秀光

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