2016 Fiscal Year Final Research Report
Exploration of tumor-promoting inflammatory immune responses and its application for cancer treatment
| Project/Area Number |
26430158
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Tumor therapeutics
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| Research Institution | University of Toyama |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | がん / 免疫 / 炎症 / 転移 |
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| Outline of Final Research Achievements |
In this study, we found IL-17A is a critical cue for escalating cancer cell malignancy. We further demonstrated the length of exposure to an inflammatory microenvironment could associate with acquiring greater tumorigenicity and IL-17A was critical for amplifying such local inflammation as observed in the production of IL-1βand neutrophil infiltration following the cross-talk between cancer and host stromal cells. We further determined that γδT cells expressing Vδ1 semi-invariant TCR initiate cancer-promoting inflammation by producing IL-17A in an MyD88/IL-23 dependent manner. Finally, we identified CD30 as a key molecule in the inflammatory function of Vδ1T cells and the blockade of this pathway targeted this cancer immune-escalation process. Collectively, these results reveal the importance of IL-17A-producing CD30+ Vδ1T cells in triggering inflammation and orchestrating a microenvironment leading to cancer progression.
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| Free Research Field |
免疫学、腫瘍生物学
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