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目的 对CD4 0配体CD15 4 (CD4 0L)在人B淋巴细胞中刺激转录因子NF κB活化进行研究。方法 应用重组CD15 4刺激EBV/LMP1阴性人RamosB细胞 ,观察对NF κBluciferase(萤光素酶 )活化的作用 ,判断CD15 4刺激对NF κB抑制蛋白IκB α、 β及 ε磷酸化和降解的影响 ,并对CD15 4刺激诱导进入细胞核NF κB亚单位进行分析。结果 CD15 4刺激 :(1)导致NF κBluciferase活性升高 ,且与CD15 4剂量正相关 ;(2 )引起细胞内IκB α、 β及 ε蛋白总量减少 ,IκB α、 β及 ε阳性细胞也明显减少 ;(3)主要诱导p5 0、p6 5及c Rel亚单位从细胞浆进入细胞核 ;(4)诱导p6 5磷酸化。结论 在人RamosB细胞中 ,CD15 4通过诱导IκB α、 β及 ε降解释放p5 0、p6 5及c Rel进入细胞核及p6 5磷酸化激活NF κB。
Objective To study the activation of transcription factor NF-κB in human B lymphocytes stimulated by CD4 0 ligand CD15 4 (CD4 0L). Methods The effect of CD15 4 stimulation on EBV / LMP1 negative human RamosB cells was observed and the effects of CD15 4 stimulation on the phosphorylation and degradation of NF κ B inhibitor IκB, And analyzed the NF-κB subunit of nucleus induced by CD15 4 stimulation. Results CD15 4 stimulation: (1) resulted in the increase of NF κBluciferase activity, and was positively correlated with the dose of CD15 4; (2) the total amount of IκB α, β and ε proteins was decreased, and the IκB α, β and ε positive cells were also significantly Decrease; (3) mainly induce the p5 0, p6 5 and c Rel subunits to enter the nucleus from the cytoplasm; (4) induce p6 5 phosphorylation. Conclusions In human RamosB cells, CD15 4 release p50, p65 and c Rel into nucleus by inducing degradation of I|ÊB|Á, |Ã and|Ã, and phosphorylation of p65 phosphorylation activate NF|ÊB.