Basic research about allergic rhinitis with CpG-DNA

共刺激分子对于调节T细胞活化和免疫应答是重要的。PD-L1已经成为一种重要的免疫调节剂，可以阻断T细胞受体信号传导。我们研究了PD-L1是否可以在CpG-DNA刺激的人B细胞中表达。CpG-DNA对人B细胞的共抑制分子配体PD-L1有较强的诱导作用。结果表明，核因子-κ B（NF-kB）信号直接参与CpG-DNA诱导的人B细胞PD-L1表达。我们试图确定CpG-DNA处理的B细胞对日本雪松花粉引起的季节性变应性鼻炎患者的Cry j 1（日本花粉抗原）刺激的人CD 4阳性细胞中Th 2细胞因子产生的影响。CpG-DNA处理的B细胞减少了CD 4阳性细胞中Cry j 1诱导的IL-5和IL-13产生。当PD-1-IG抑制PD-1与PD-L1的结合时，该嵌合分子逆转了先前描述的IL-5和IL-13产生的减少。这些结果表明，CpG-DNA诱导人B细胞中的共抑制分子配体PD-L1表达，并且PD-L1可以抑制Cry j 1刺激的CD 4阳性细胞中的Th 2细胞因子产生，而CpG-DNA增加Th 1细胞因子产生并减少可以促进Th 2炎症反应的共刺激分子配体的表达。

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.