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目的 :研究细胞粘着分子 1(ICAM 1)和血管细胞粘着分子 1(VCAM 1)单抗对rIL 2活化的脐血淋巴细胞粘附人脐静脉内皮细胞 (HUVEC)的机理。方法 :①利用 2 4孔板培养HUVEC ,在相应孔中分别加入ICAM 1和VCAM 1单抗 ,30min后测定活化的脐血淋巴细胞和未活化的淋巴细胞粘附百分率 ;②采用桥联酶标法 (APAAP)测定粘附细胞的表型。结果 :①ICAM 1和VCAM 1单抗 (2 0mg/L)均可明显降低rIL 2活化的淋巴细胞的粘附 ,前者使粘附率由 56 54%降至 4 1 6 0 % (P <0 .0 5) ;后者使粘附率降至 30 30 % (P <0 .0 5) ;②粘附细胞的表型分析结果表明 ,ICAM 1单抗可降低CD8+ 细胞的粘附 ,增加CD4 + 细胞的粘附 ,对CD56 + 细胞的粘附无明显影响 ,而VCAM 1单抗则增加CD8+ 细胞的粘附 ,降低CD56 + 细胞的粘附 ,对CD4 +细胞无明显影响。结论 :粘着分子ICAM 1和VCAM 1参与活化脐血淋巴细胞粘附HUVEC的调控 ,其抗体虽可明显降低活化脐血淋巴细胞对HUVEC的粘附 ,但机理不同
AIM: To investigate the mechanism of rIL 2-activated cord blood lymphocytes adhering to human umbilical vein endothelial cells (HUVECs) by ICAM-1 and VCAM 1 monoclonal antibodies. Methods: ① HUVECs were cultured in 24-well plates, ICAM 1 and VCAM 1 McAbs were respectively added to the corresponding wells, and the percentage of activated cord blood lymphocytes and unactivated lymphocytes was measured after 30 min. Method (APAAP) to determine the phenotype of adherent cells. Results: ①ICAM 1 and VCAM 1 mAb (20 mg / L) significantly decreased the adhesion of lymphocytes activated by rIL 2. The former reduced the adhesion rate from 56 54% to 41 6 0% (P <0. (P <0.05). (2) Phenotypic analysis of adherent cells showed that ICAM 1 mAb could reduce the adhesion of CD8 + cells and increase the percentage of CD4 + Cell adhesion had no significant effect on CD56 + cell adhesion, whereas VCAM 1 mAb increased CD8 + cell adhesion and decreased CD56 + cell adhesion with no significant effect on CD4 + cells. CONCLUSION: Adhesion molecule ICAM 1 and VCAM 1 are involved in the regulation of HUVEC adhesion activated by umbilical cord blood. Although the antibody can significantly reduce the adhesion of activated cord blood lymphocytes to HUVEC, the mechanism is different