2011 Fiscal Year Final Research Report
Basic research about allergic rhinitis with CpG-DNA
| Project/Area Number |
22791581
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Otorhinolaryngology
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| Research Institution | University of Fukui |
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Principal Investigator |
KUBO Seita 福井大学, 医学部・附属病院, 助教 (80401983)
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| Project Period (FY) |
2010 – 2011
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| Keywords | CpG / B細胞 / PD-L1 / T細胞 / 共刺激分子 |
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| Research Abstract |
Co-stimulatory molecules are important for regulating T cell activation and immune response. PD-L1 has emerged as an important immune modulator that can block T cell receptor signaling. We have investigated whether PD-L1 could be expressed in human B cells stimulated by CpG-DNA. CpG-DNA strongly induced the coinhibitory molecule ligand, PD-L1 of human B cells. Results show that nuclear factor-kappa B(NF-kB) signaling is involved directly in CpG-DNA-induced PD-L1 expression in human B cells. We sought to determine the effect of CpG-DNA-treated B cells on Th2 cytokine production in Cry j 1(Japanese pollen antigen)-stimulated human CD4-positive cells from patients with seasonal allergic rhinitis caused by Japanese cedar pollen. CpG-DNA-treated B cells reduced Cry j 1-induced IL-5 and IL-13 production in CD4-positive cells. When the binding of PD-1 to PD-L1 was inhibited by PD-1-Ig, this chimera-molecule reversed the previously described reductions in IL-5 and IL-13 production. These results indicate that CpG-DNA induces the coinhibitory molecule ligand PD-L1 expression in human B cells and PD-L1 can suppress Th2 cytokine production in Cry j 1-stimulated CD4-positive cells, while CpG-DNA increased Th1 cytokine production and reduced the expression of costimulatory molecule ligands that can promote Th2 inflammatory responses.
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Research Products
(3 results)
