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出 处:《中国免疫学杂志》1999年第7期302-304,共3页Chinese Journal of Immunology
基 金:国家自然科学基金
摘 要:目的:研究柯萨基B3病毒(CoxB3)感染对内皮细胞表面ICAM1表达的诱导作用,及对内皮细胞与单个核细胞粘附的影响,探讨病毒性心肌炎心肌细胞免疫损伤的机理。方法:采用流式细胞仪分析内皮细胞ICAM1表达;粘附试验和单克隆抗体抑制试验观察单个核细胞与内皮细胞的粘附。结果:100和400TCID50/mlCoxB3感染内皮细胞24和48h,均可显著增加单个核细胞与内皮细胞的粘附(P<001),分别为对照组的18和25倍。经流式细胞仪分析证实,CoxB3感染可以诱导内皮细胞ICAM1表达增加,阳性细胞数增多。用抗ICAM1和抗LFA1单克隆抗体均可部分阻断单个核细胞与CoxB3感染内皮细胞的粘附,抗ICAM1单抗的抑制作用较抗LFA1单抗更为明显。结论:CoxB3可以通过感染内皮细胞上调膜ICAM1的表达,促进单个核细胞与内皮细胞的粘附。Objective: To investigate the inductive effects of coxsackie B3 virus (Cox B3) infection on ICAM1 expression of cultured cardiac microvascular endothelial cells and adhesion to mononuclear cells. Methods: Flow cytometry on a FACScan to analyze expression on cardiac microvascular endothelial cells, adhesion assay and monoclonal antibodies inhibition assay to observe the adhesion of mononuclear cells to endothelial cells. Results: Adhesion of rat mononuclear cells to endothelial cells was significantly enhanced following Cox B3 infection for 24 or 48 h (P<0.01) Cox B3 infection significantly increased ICAM1 expression on cultured endothelial cells by flow cytometry. Adhesion was reduced by blocking monoclonal antibodies (McAb) to endothlial cells ICAM1 or mononuclear cells LFA1, the blocking effect of McAb against ICAM1 was more obvious than that of McAb to LFA1. Conclusion: Cox B3 infections of cardiac microvascular endothelia cells can increase surface expression of ICAM1, and promote inf
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