论文部分内容阅读
目的研究天花粉蛋白（Ｔｋ）抑制Ｔ细胞增殖的作用机理。方法以抗ＣＤ３的ＭｃＡｂ刺激ＪｕｒｋａｔＴ细胞增殖，以３Ｈ－ＴｄＲ同位素掺入法观察Ｔｋ对其抑制作用。用免疫沉淀和免疫印迹法测定胞浆蛋白酪氨酸磷酸化情况。结果Ｔｋ能够抑制ＣＤ３ＭｃＡｂ刺激的ＪｕｒｋａｔＴ细胞的增殖，并且经Ｔｋ脉冲处理后的ＪｕｒｋａｔＴ细胞对ＣＤ３ＭｃＡｂ活化作用的反应降低。深入分析后发现，在Ｔｋ作用下胞浆蛋白酪氨酸磷酸化水平降低，经ＰＬＣγ１免疫沉淀后，发现ＰＬＣγ１的磷酸化也能够被Ｔｋ作用所抑制。结论Ｔｋ对Ｔ细胞活化的抑制涉及并经由ＴＣＲ的激活信号传导，其机理与阻断胞浆蛋白酪氨酸激酶磷酸化有关
Objective To study the mechanism of Tk inhibition of T cell proliferation. Methods The proliferation of Jurkat T cells was stimulated with anti-CD3 McAb. The inhibitory effect of Tk was observed by isotope incorporation of 3H-TdR. Cytosolic protein tyrosine phosphorylation was measured by immunoprecipitation and immunoblotting. As a result, Tk was able to inhibit the proliferation of CD3McAb-stimulated Jurkat T cells, and the Tk-pulsed Jurkat T cells were less responsive to the activation of CD3McAb. In-depth analysis found that under the action of Tk decreased protein tyrosine phosphorylation level, after PLCγ1 immunoprecipitation, we found that PLCγ1 phosphorylation can also be Tk inhibition. Conclusions Tk inhibition of T cell activation involves signaling via TCR activation, and its mechanism is related to blocking the phosphorylation of cytoplasmic protein tyrosine kinase