2015 Fiscal Year Final Research Report
Analysis of the mechanism of MCL-mediated activation of acquired immune responses.
| Project/Area Number |
25460593
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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 | Saga University (2014-2015)
Kyushu University (2013) |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | C型レクチン受容体 |
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| Outline of Final Research Achievements |
Two C-type lectin receptors, Mincle and MCL, are required for immune responses against mycobacterial glycolipid, TDM. We demonstrate that MCL interacts with Mincle to promote its surface expression. After LPS or zymosan stimulation, MCL-deficient BMDCs had a lower level of Mincle protein expression. Meanwhile, BMDCs from MCL transgenic mice showed an enhanced level of Mincle expression on the cell surface. MCL was associated with Mincle through the stalk region and this region was necessary and sufficient for the enhancement of Mincle expression. This interaction was mediated by the hydrophobic repeat of MCL, as substitution of four hydrophobic residues with serine abolished the function to enhance the Mincle expression. This mutant failed to restore the defective TDM responses in MCL-deficient BMDCs. These results suggest that MCL positively regulates Mincle expression through protein–protein interaction via its stalk region, thereby magnifying Mincle-mediated signaling.
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| Free Research Field |
免疫学
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