| Project/Area Number |
16K18449
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor therapeutics
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Research Collaborator |
MATSUSHITA TAKASHI 金沢大学, 附属病院, 講師 (60432126)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2017: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 悪性黒色腫 / 制御性B細胞 / 免疫療法 / 腫瘍免疫 / IL-10 / Regulatoly B細胞 |
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| Outline of Final Research Achievements |
In tumor immunity, the participation of IL-10-producing regulatory B cell (Breg) which suppresses several immune responses is unclear. Here we demonstrated that B16F10 melanoma growth was increased in B cell-specific phosphatase and tensin homolog (PTEN)-deficient mice in which Breg subset is expanded. More than 50% of the tumor-infiltrating B cells consisted of Bregs in both B cell-specific PTEN-deficient mice and control mice. The number of tumor-infiltrating Bregs was significantly increased in B cell-specific PTEN-deficient mice. Although we have previously identified 2 Breg subsets derived from marginal zone Bregs and B1 Bregs, most of tumor-infiltrating Bregs consisted of B1 Bregs but not MZ Bregs. Adoptive transfer of B1 B cells increased melanoma growth while non-B1 B cells had no effect. Thus, B1 Bregs negatively regulate tumor immunity against melanoma.
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