| Project/Area Number |
25670236
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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 |
Immunology
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| Research Institution | Kansai Medical University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
OHTANI Masashi 東邦大学, 理学部, 講師 (20383713)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | B細胞分化 / mTORC1シグナル / 腸内細菌 / mTORC1 / IgA |
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| Outline of Final Research Achievements |
Mice with a B cell-specific deletion of Raptor (RaptorB-/- mice), an essential component of mammalian target of rapamycin complex 1 (mTORC1), had a developmental arrest at the pro-B cell stage in the bone marrow (BM) and consequently failed to produce detectable levels of IgM and IgG. However, RaptorB-/- mice still produced gut-associated IgA required for controlling gut microbiota. Unexpectedly, RaptorB-/- B cells underwent somatic hyper mutation (SHM) in the gene encoding IgA despite the fact that T follicular helper (TFH) cells were absent. Our findings reveal a gut-associated mTORC1-independent differentiation program of IgA+ B cells, which plays a crucial role in maintaining intestinal homeostasis.
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