| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2010: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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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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