2011 Fiscal Year Final Research Report
Immunological Abnormality caused by MARCH I/c-MIR 2 deficiency
| Project/Area Number |
21590422
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | The Institute of Physical and Chemical Research |
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Principal Investigator |
HOSHINO Mari 独立行政法人理化学研究所, 感染免疫応答研究チーム, 研究員 (10313511)
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| Project Period (FY) |
2009 – 2011
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| Keywords | E3ユビキチンリガーゼ / 樹状細胞 |
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| Research Abstract |
We have investigated the physiological function of MARCH(membrane associated RING-CH protein) family. So far, we reported that MARCH-I-deficient cDCs and B cells accumulated MHC II and B7-2 and exhibited low Ag-presenting ability for exogenous Ags. Furthermore, MHC II, but not B7-2, was required for impaired cDC function induced by loss of MARCH-I in vivo. On this study we found that conditional inhibition of MARCH-I induced natural Treg-dependent apoptosis of mature DCs due to loss of MHC II ubiquitination. Our results suggest that maturation of DCs induces their "suicide" by facilitating recognition by Tregs, which is induced by loss of pMHC II ubiquitination in the steady state.
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[Journal Article] CD83 increases MHC II and CD86 on dendritic cells by opposing IL-10-driven MARCH1-mediated ubiquitination and degradation2011
Author(s)
Tze LE, Horikawa K, Domaschenz H, Howard DR, Roots CM, Rigby RJ, Way DA, Ohmura-Hoshino M, Ishido S, Andoniou CE, Degli-Esposti MA, Goodnow CC.
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Journal Title
J Exp Med
Volume: 208
Pages: 149-165
Peer Reviewed
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