2017 Fiscal Year Final Research Report
A role of Arl8b for the development of SLE
| Project/Area Number |
26293083
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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 |
Experimental pathology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Keywords | 全身性エリテマトーデス / Arl8b / 自己免疫疾患 / 形質細胞様樹状細胞 / Toll-like Receptor 7 |
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| Outline of Final Research Achievements |
lysosomal small G protein Arl8b is associated with Toll-like Receptor 7(TLR7), which is an RNA sensor recognizing viral or bacterial RNA in endosome or lysosome. We clarified that Arl8b is essential for the development of Systemic lupus erythematosus (SLE) in TLR7 and type 1 Interferon dependent SLE mouse models, BXSB.Yaa and TMPD-induced SLE. We reported that Arl8b plays an important role for TLR7 dependent type 1 Interferon expression in pDC. We also analyzed another type of SLE model, MRL/lpr. It is not TLR7 and type 1 dependent SLE model so much. We found that Arl8b is also essential for the development of SLE in TLR7 and type 1 Interferon independent mechanism in MRL/lpr. Arl8b controls regulatory T cells and the development of SLE in this model.
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| Free Research Field |
炎症免疫学
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