嗜酸性粒细胞（EOS）是变应性鼻炎主要效应细胞，G蛋白偶联受体（CCR3)是EOS表面受体，其与嗜酸性粒细胞趋化因子（Eotaxin)结合激活下游信号通路在EOS活化迁移中起重要作用，我们研究发现RNAi沉默CCR3可抑制EOS由骨髓向鼻粘膜迁移，但其作用机制尚未完全阐明。脂酰肌醇-3-激酶（PI3K）是G蛋白偶联受体下游信号通路, 我们预实验发现：抑制PI3K通路可减少EOS的迁移。而CCR3是否通过PI3K影响EOS由骨髓向鼻粘膜迁移尚未见报道。为此,我们提出假说敲除骨髓CCR3可抑制Eotaxin/CCR3轴而影响PI3K通路，从而使EOS由骨髓-外周血-鼻粘膜迁移过程受抑制而减轻变应性鼻炎发病。为验证这一假说，我们将运用Cre-LoxP技术敲除骨髓CCR3，采用PI3K抑制剂、QPCR等手段探讨该方法对变应性鼻炎EOS迁移机制影响，为建立可能的干预手段寻找到新的分子靶点。

Eosnophils (EOS) is the mainly effector cells of allergic rhinitis (AR), G-protein-coupled receptor (CCR3), which located on the surface of EOS, will activate a downstream signaling pathway by binding with eotaxin, a chemotactic factor of EOS, play a critical role in the activation and migration of EOS cascade reactions, but the mechanism of these multi-cascade reaction still on open debate. Our previous research demonstrated that silence CCR3 through RNAi inhibited EOS migration from bone marrow to the nasal mucous, activation and degranulation, and then reduced the inflammation reactions in nasal mucous. Phosphatidlyinositol-3-kinase (PI3K) is a main downstream signaling of G-protein-coupled receptor, plays an important role in the EOS migration, the role of CCR3 affect EOS migration by influencing downstream signaling PI3K in the pathogenesis is not yet clear. In this case, we propose hypothesis that: CCR3 knock out from the bone marrow might inhibit Eotaxin/bone axle and inactivate the signaling pathways of PI3K,therefore, the migration process of EOS from bone marrow to peripheral blood to nasal mucosa might be stopped and reduce the allergic rhinitis symptoms. To verify this hypothesis,We will use the Cre-Loxp to knock out CCR3 from the bone marrow, allergic rhinitis mouse model, PI3K inhibitor, Western blot and QPCR technique to explore the change of Eos migration mechanism.So that ,we can find a new molecular target for treatment of allergic rhinitis .