Effect of protein kinase C on proliferation and apoptosis of T lymphocytes in idiopathic thrombocytopenic purpura children.

Effect of protein kinase C on proliferation and apoptosis of T lymphocytes in idiopathic thrombocytopenic purpura children.
复制标题

DOI:
--
复制
发表时间:
2005-06
影响因子:
24.1
通讯作者:
Chang-lin Wu;Fang Liu;Xuemin Zhou;Zhengwei Cheng;Xiao-meng Yang;Hong Xiao;Qun Chen;K. Cai
Chang-lin Wu;Fang Liu;Xuemin Zhou;Zhengwei Cheng;Xiao-meng Yang;Hong Xiao;Qun Chen;K. Cai
中科院分区:
医学1区
文献类型:
--
作者:
Chang-lin Wu;Fang Liu;Xuemin Zhou;Zhengwei Cheng;Xiao-meng Yang;Hong Xiao;Qun Chen;K. Cai

文献摘要

被引文献

相似文献

文献表明,特发性血小板减少性紫癜(ITP)患儿T淋巴细胞增殖和凋亡异常。然而,潜在的调节机制,特别是在信号转导方面仍然未知。本文报道了外周血T淋巴细胞蛋白激酶C (PKC)活性的变化及其对T淋巴细胞增殖和凋亡的影响。我们发现,在ITP儿童中,PKC的激活剂(PMA)和抑制剂(H-7)对T淋巴细胞增殖和凋亡有显著影响,但在健康儿童中变化不大。ITP患儿PKC活性显著增强,CD3+T、CD4+T和CD8+T细胞上FasL表达增加,PKC活性与T细胞上FasL表达呈正相关。PKC活性与血小板计数呈负相关。综上所述,我们的研究结果表明PKC激活可能增强T淋巴细胞活性,抑制T细胞凋亡,并参与血小板损伤,作为ITP免疫发病机制的一个相关机制。
It is well-documented that T lymphocyte proliferation and apoptosis are abnormal in idiopathic thrombocytopenic purpura (ITP) children. However, the underlying regulation mechanisms especially in terms of signal transduction remain unknown. In this paper, we reported the changes of protein kinase C (PKC) activity in peripheral blood T lymphocytes and the effect of PKC on T lymphocyte proliferation and apoptosis. We demonstrated that in ITP children, the activator (PMA) and inhibitor (H-7) of PKC affected on T lymphocyte proliferation and apoptosis dramatically, but they altered little in healthy children. PKC activity was significantly enhanced in ITP children together with an increased expression of FasL on CD3+T, CD4+T and CD8+T cells, resulting in a positive correlation between PKC activity and the expression of FasL on T cells. While the PKC activity and the platelet count were negatively correlated. Taken together, our findings suggest that the PKC activation may enhance T lymphocytes activity, suppress T cell apoptosis and be involve in thrombocytes damage as a mechanism related to immune pathogenesis of ITP.