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2016 Fiscal Year Final Research Report

The detrimental effect of soluble IL-6 receptor on CD4 T cell-mediated anti-tumor immune responses

Research Project

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Project/Area Number 26430165
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Tumor therapeutics
Research InstitutionKumamoto University

Principal Investigator

Tsukamoto Hirotake (塚本博丈)  熊本大学, 大学院生命科学研究部(医), 助教 (10433020)

Research Collaborator Fujieda Koji  熊本大学, 生命科学研究部, リサーチアシスタント
Ikeda Tokunori  熊本大学, 医学部付属病院, 病院職員 (00613530)
Nakayama Hideki  熊本大学, 生命科学研究部, 教授 (70381001)
Araki Kimi  熊本大学, 生命資源研究・支援センター, 教授 (90211705)
Senju Satoru  熊本大学, 生命科学研究部, 准教授 (50274709)
Nishimura Yasuharu  熊本大学, 生命科学研究部, 教授 (10156119)
Project Period (FY) 2014-04-01 – 2017-03-31
Keywords抗腫瘍免疫応答 / 炎症 / T細胞 / IL-6 / 免疫抑制 / がん免疫療法 / sIL-6R
Outline of Final Research Achievements

It is well known that pro-inflammatory cytokine IL-6 produced by tumor cells promotes their own survival, therefore is a poor prognostic factor in cancer patients. In terms of anti-tumor immune responses, Th1 differentiation of tumor-specific CD4 T cells is attenuated in tumor-bearing animals in an IL-6-dependent fashion. In this study, we investigated the immune-suppressive effects of IL-6 signaling by focusing on IL-6 trans-signaling mediated thorough a soluble form of IL-6 receptor (sIL-6R).
We found that accompanied by the systemic increase of sIL-6R in cancer patients, blunted activity of sIL-6R restored the Th1 responses, their helper activity toward CD8 T cells, and anti-tumor activity in tumor-bearing mice. Our findings suggest the implication of the increase in IL-6 signaling as an adverse event counteracting tumor-specific Th1 generation, and that sIL-6R is considered for a rational target to improve the effectiveness of T cell-mediated cancer immunotherapy.

Free Research Field

免疫学

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Published: 2018-03-22  

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