Molecular mechanism of MHC trogocytosis
| Project/Area Number |
16K15112
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Biological pharmacy
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| Research Institution | Tohoku University |
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Principal Investigator |
Nakayama Masafumi 東北大学, 学際科学フロンティア研究所, 准教授 (20453582)
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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 |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 樹状細胞 / MHC / トロゴサイトーシス / MHCクラスI |
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| Outline of Final Research Achievements |
Cross-presentation of dying cell antigens is crucial for the induction and/or regulation of cytotoxic T lymphocytes. This process is mediated by a certain DC subset such as mouse CD8alpha+ DCs that can efficiently engulf dying cells and present these exogenous antigens with the endogenous MHC class I molecules (MHCI). In addition to this cross-presentation, several recent studies have revealed that DCs can acquire MHCI from neighboring cells, and present the pre-formed antigen peptide-MHCI complexes without requiring any further processing, which is recently called cross-dressing. However, the physiological role of cross-dressing is not fully understood. We here found that trogocytosis of dying cell-derived MHCI by splenic DCs is independent on Tim-3, a phosphatidylserine receptor,-mediated phagocytosis, and that cross-dressing contributes to the early T cell proliferation.
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Report
(3 results)
Research Products
(15 results)
