中文摘要：

目的 探讨重组人粒细胞集落刺激因子（rhG—CSF）动员对CD4^＋T淋巴细胞表面分子CXCR4和淋巴细胞功能相关抗原1（LFA-1）所介导功能和相关信号机制的影响。方法 在rhG-CSF动员前和动员后第5天抽取供者外周血，用三色荧光标记检测动员前后CD4^＋T淋巴细胞LFA-1和CXCR4的表达率，并应用免疫磁性分选法分离纯化CD4^＋T淋巴细胞，检测动员前后CD^4＋T淋巴细胞对基质细胞衍生因子10α（SDF=1α）的迁移能力和对细胞间黏附分子1（ICAM-1）的黏附能力。 结果 rhG—CSF动员前后CD4^＋T淋巴细胞的LFA-1（CD11a）和CXCR4表达率差异无统计学意义（P〉0．05），动员前后CD4^＋T细胞LFA-1表达率均为100％；动员前CD4^＋T淋巴细胞CXCR4表达率为（84．58±20．31）％，动员后为（81．23±22．46）％。动员前后CD4^＋T淋巴细胞向SDF-1α的4h迁移率分别为（28．5±10．3）％和（31．2±8．9）％，差异无统计学意义（P〉0．05）；动员前后CD4^＋T淋巴细胞在CD3单抗作用下对ICAM-1的黏附率分别为（85．59±14．21）％和（61．45±15．07）％，动员前显著高于动员后（P〈0．05）。结论 rhG—CSF动员不影响CD4^＋T淋巴细胞LFA-1和CXCR4的表达，但影响CD4^＋T淋巴细胞通过LFA-1对ICAM-1的黏附能力。

英文摘要：

Objective To explore the impact of mobilization with recombinant human granunocyte clonony stimulated factor （rhG-CSF） on the migration and adhesive function and their related signal mechanism mediated by the CXCR4 and lymphocyte function antigen-1 （ LFA-1 ） molecules on the surfaces of CD4^＋ T cells. Methods Before and at day 5 on rhG-CSF mobilization, the expression rates of CXCR4 and LFA-1 （CD11 a） on CD4^＋ T cells in the peripheral blood were detected by tricolor fluorecenee labeling, and the migration and adhesive activities of CD4^＋ T cells to stroma cell-derived factor 1 α （ SDF-1 α） and intercellular adhesion molecule-1 （ ICAM-1 ） were also tested. Results The expression of CXCR4 on CD4^＋ T lymphocytes was （84.58 ± 20.31 ）% before mobilization and （81.23 ± 22.46 ）% at day 5 on mobilization. The expression of LFA-1 on CD4^＋ T lymphocytes before and at day 5 on mobilization was 100%. There was no significant difference in the expression CXCR-4 and LFA-1 on CD4^＋ T lymphocytes whether mobilization （ P 〉 0.05 ）. SDF-1α induced 4 hours＇ CD4^＋T cells migration didn＇t change markedly before and after mobilization [ （28.5 ± 10.3）% vs （31.2 ±8.9）% ] （P〉0. 05）. The adhesive activity of CD4^＋T cells to ICAM-1 was decreased from （ 85.59 ± 14.21 ） % to （ 61.45 ± 15.07 ） % after mobilization （ P 〈 0.05 ）. Conclusions The expression of CXCR4 and LFA-1 on CD4^＋ T lymphocytes didn＇t change markedly during rhG-CSF mobilization, but the adhesive activity of CD4^＋T cells to ICAM-1 was frustrated after that.