Regulation of differentiation of the small intestinal lamina proprial CX3CR1-positive cells by the Notch signal.
| Project/Area Number |
24890146
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Immunology
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| Research Institution | The University of Tokushima |
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Principal Investigator |
ISHIFUNE Chieko 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 助教 (80632645)
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| Project Period (FY) |
2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 抗原提示細胞 / 粘膜免疫 / 分化 / Notchシグナル / 小腸 / 粘膜固有層 / 粘膜免疫応答 |
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| Research Abstract |
From our research, we observed the CX3CR1+sLPC were markedly decreased and the CD11c+sLPC were increased in small intestinal lamina propria by CD11c-dependent deletion of Rbpj. We found that Notch1 and/or 2 are essential receptor of the canonical Notch-RBP-J signal required for the differentiation of CX3CR1+sLPC. The Notch ligands supplied by intestinal epithelial cells were not essential. The CD11clow sLPC differentiated from CX3CR1+monocytes in Rbpjdeficient mice is not a precursor but one subtype of CX3CR1+cell. Our data suggest that the canonical Notch1 and/or Notch2-RBP-J signaling affects the homeostasis of intestinal immune responses via regulating the differentiation of CX3CR1+sLPC
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Report
(2 results)
Research Products
(9 results)
