再生障碍性贫血（简称再障）是一种以造血组织为靶细胞的自身免疫性疾病，T细胞在骨髓中介导的造血干/组细胞的破坏和凋亡是导致骨髓造血功能衰竭的根本原因。我们前期的体外研究发现，再障患者T细胞表面CX3CR1的表达明显升高，其相应的配体CX3CL1在骨髓血浆中亦明显升高，随着有效的治疗，CX3CR1的表达明显下降。体外阻断CX3CL1与CX3CR1的相互作用可有效地阻断再障患者T细胞的趋化与粘附作用。推测CX3CL1与CX3CR1介导T细胞迁移至骨髓，与再障的发生、发展密切相关。基于上述的研究成果，本项目将以免疫介导的再障小鼠模型为研究对象，深化前期研究工作，通过体内阻断CX3CL1/CX3CR1轴，观察对于T细胞向骨髓迁移及造血功能恢复的影响。预期的研究结果可能成为再障潜在的药物治疗靶点，从而为再障的治疗提供新的思路和线索。

Aplastic anemia (AA) is an autoimmune disease targeted hematopoietic tissue. T-cell-mediated destruction and apoptosis of hematopoietic stem and progenitor cells is considered the root cause for bone marrow failure. Our previous studies in vitro have found that in AA patients，the expression of CX3CR1 was significantly increased on the T cells, and its corresponding ligand-CX3CL1 was also increased in bone marrow plasma, with effective treatment, the high expression of CX3CR1 was significantly decreased, as well as, chemotaxis and adhesion of T cells can be effectively inhibited by blocking interaction of CX3CL1 and CX3CR1. Thus, we have concluded that CX3CL1/CX3CR1-mediated T cells recruitment into bone marrow is closely related with development of AA. Based on above findings, we have planned to take the immune mediated mouse model of AA as research objects for deepening the previous works and observe the influence of the T cells migration into bone marrow and hematopoietic recovery by blocking the interaction of CX3CL1 and CX3CR in vivo. Expecting results may be a potential target for drug therapy of AA and then provide new ideas and clues for treatment of AA.