Novel immune regulation through regulated MHC II ubiquitination
| Project/Area Number |
24390122
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Immunology
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| Research Institution | Showa Pharmaceutical University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
NAOE Yoshinori 独立行政法人国立長寿医療センター, 老化機構研究部免疫研究室, 室長 (50392048)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥18,590,000 (Direct Cost: ¥14,300,000、Indirect Cost: ¥4,290,000)
Fiscal Year 2014: ¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
Fiscal Year 2013: ¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
Fiscal Year 2012: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
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| Keywords | ユビキチン / MHC class II / 樹状細胞 / 抗原提示 / CD86 / 寛容 / IgE |
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| Outline of Final Research Achievements |
pMHC II are continuously replaced with newly generated pMHC II through continuous ubiquitination by MARCH-I. The recycling of pMHC II is thought to be necessary for quick immune response against newly invading pathogens. In contrast, infectious stimuli inhibit recycling of pMHC II through inhibition of MARCH-I-mediated ubiquitination,thereby initiating immunity. Therefore, we are challenging to have experimental evidence for the hypotheses. We have generated the mice whose pMHC II is continuously ubiquitinated. This mouse showed impairment of immune response. In addition, the number of lymphocyte was reduced in the periphery. In MHC II-deficient mice, the number of leukocyte including lymphocyte was increased in the periphery, indicating that reduction of lymphocyte number is not simply due to down-regulation of MHC II in this mouse. Our results support the present hypothesis and suggest that regulated ubiquitination of pMHC II requires homeostasis of lymphocytes.
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Report
(4 results)
Research Products
(12 results)
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[Journal Article] MITOL regulates endoplasmic reticulum-mitochondria contacts via Mitofusin2.2013
Author(s)
Sugiura, A., Nagashima, S., Tokuyama, T., Amo, T., Matsuki, Y., Ishido, S., Kudo, Y., McBride, H.M., Fukuda, T., Matsushita, T., Inatome, R., and C Yanagi, S.
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Journal Title
Mol. Cell
Volume: 51
Issue: 1
Pages: 1-15
DOI
Related Report
Peer Reviewed
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