人类急性T淋巴细胞白血病（T-ALL）细胞穿过血脑屏障（BBB）迁移入脑是其脑转移的前提。我们前期工作发现：T-ALL四种细胞系细胞MIP-1α表达均高于正常人T淋巴细胞分泌的MIP-1α，尤以Jurkat最显著。我们选择Jurkat细胞作为研究T-ALL细胞穿过BBB机制的模式细胞,Jurkat（MIP-1α siRNA）对HBMECs黏附和跨内皮迁移率下降；Jurkat（MIP-1α siRNA）抑制了HBMECs部分黏附分子表达上调。基于此本项目将进一步分析MIP-1α对内皮黏附分子表达的影响；解析黏附分子在T-ALL Jurkat细胞系细胞黏附HBMECs中的作用；明确HBMECs上与MIP-1α相结合引起黏附分子表达上调的受体，探寻T-ALL细胞穿过BBB入脑的机制。可望从细胞和分子水平阐明T-ALL细胞穿过血脑屏障的机制，为防治其脑转移提供新的干预靶点。

T-cell acute lymphoblastic leukemia （T-ALL）cells penetrate the BBB, and migrate to CNS which plays an important role in brain metastases. Our previous results showed the four T-ALL cell have significantly higher macrophage inflammatory protein-1α (MIP-1α) expression than of normal T cells,especially Jukat cell line.The adhesion and migration ability of Jukat(MIP-1α siRNA) to HBMECs reduced,and Jurkat(MIP-1α siRNA)induced adhesion molecules expression in HBMECs. Based on these results, this study is to investigate the molecular mechanism of endothelial adhesion molecules expression up-regulated by MIP-1α, and further analysis that the role of endothilial adhesion molecules in T-ALL cells adhesion HBMECs and search the overexpressed receptor of MIP-1α on HBMECs to anlalyzed the mechenism of T-ALL cells penetrate BBB. This study is expected from the cellular and molecular level to explain the mechanisms of T-ALL cells crossing through the blood brain barrier ,which may provide the new intervention target for the prevention of the metastatic brain.