2015 Fiscal Year Final Research Report
Elucidation of Tumor Immune Escape Mechanisms Promoted Lymph Node Metastasis
| Project/Area Number |
25461971
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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 |
General surgery
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| Research Institution | Akita University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
MINAMIYA Yoshihiro 秋田大学, 大学院医学系研究科, 教授 (30239321)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | TGF-β1 / 樹状細胞 / センチネルリンパ節 / リンパ節転移 / がん免疫逃避機構 |
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| Outline of Final Research Achievements |
Transforming growth factor (TGF)-βis known to be produced by progressor tumors and to immobilize dendritic cells (DCs) within those tumors. Moreover, although TGF-β1 has been shown to promote tumor progression, there is still no direct evidence as to whether TGF-β1 is able to directly induce distant metastasis. To address that issue and investigate the mechanism by which TGF-β1 suppresses DC, B cell, and T cell activity in tumor draining lymph node (TDLN), we subdermally inoculated mouse ears with squamous cell carcinoma cells stably expressing TGF-β1 or empty vector (mock). Two weeks after inoculation, the mice were sacrificed, and the neck TDLN was excised. TDLN from mice inoculated with TGF-β1 clone showed significantly lower levels of CCL19, CCL21, and IL-4 mRNA than mock. In addition, we found that DCs, B cells, CD40L+ Tfh cells, and CD4+CXCR5+CCR7- subset were reduced in mice inoculated with TGF-β1 clone. These findings suggest TGF-β1 inhibits early immunological memory.
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| Free Research Field |
胸部外科学
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