Regulatory mechanism for the differentiation and function of innate-like B cells
| Project/Area Number |
26460570
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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 |
Immunology
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| Research Institution | Niigata University |
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Principal Investigator |
Touma Maki 新潟大学, 自然科学系, 助教 (40542246)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | B細胞 / 自然免疫 / 自然免疫シグナル / 炎症応答 / 自己免疫 / 自己抗体 / B-1細胞 / 自然抗体 |
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| Outline of Final Research Achievements |
Peritoneal B-1 cells and splenic marginal zone B cells that show rapid response to innate immune signals are called innate-like B cells. We investigated regulatory mechanisms for the differentiation and function of innate-like B cells focused on the role of IκBNS that is an atypical IκB molecule necessary for differentiation of these B cells. As a result, it was suggested that IκBNS is involved in the control of signal intensity via B cell receptor, which is considered important for differentiation of B-1 cells and marginal zone B cells. Innate-like B cells are also known as IL-10-producing B cell subsets. In this study, it was revealed that IκBNS is selectively required for IL-10 production in B cells responding to Toll-like receptor signals.
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Report
(4 results)
Research Products
(6 results)
