2016 Fiscal Year Final Research Report
Analysis on the mechanism of immune regulation by CD4+ conventional dendritic cells in the development of autoimmune diseases
| Project/Area Number |
26860337
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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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) |
2014-04-01 – 2017-03-31
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| Keywords | 樹状細胞 |
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| Outline of Final Research Achievements |
Dcir2-/- CD4+ cDCs showed a higher secretion of proinflammatory cytokines and an enhanced T-cell priming after stimulation with TLR ligands than wild-type (WT) CD4+ cDCs. Furthermore, Dcir2-/- mice exhibit a hyperinflammatory response associated with the excessive production of cytokines. On antigenic immunization, Dcir2-/- mice showed a more enhanced autoimmune pathogenesis than WT mice. Thus, our findings suggest that DCIR2 provides an inhibitory signal for the fine-tuning of the function of CD4+ cDCs to maintain immune homeostasis and prevent autoimmune diseases.
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| Free Research Field |
免疫学
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