2015 Fiscal Year Final Research Report
Analysis of the role of DCIR2 in the function of CD4+conventional dendritic cells
| Project/Area Number |
25293117
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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 | University of Miyazaki |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | 樹状細胞 / 自然免疫 / 適応免疫 / T細胞 / 機能抑制分子 |
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| Outline of Final Research Achievements |
Here, we show that DCIR2 is a regulatory receptor for the activation of CD4+cDCs that impairs inflammation and T-cell immunity. Dcir2-/-CD4+cDCs show enhanced cytokine production and T-cell priming following TLR-mediated activation. Furthermore, Dcir2-/- mice exhibit TLR-mediated hyperinflammation. Upon antigenic immunization,Dcir2-/- mice show not only augmented T-cell responses but also progressive autoimmune pathogenesis. Thus, our findings highlight roles of Clec4A4 in regulation of the function of CD4+cDCs for control of the magnitude and quality of immune response.
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| Free Research Field |
免疫学
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