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It is well-documented that T lymphocyte proliferation and apoptosis are abnormal in idiopathic thrombocytopenicpurpura(ITP)children.However,the underlying regulation mechanisms especially in terms of signal transductionremain unknown.In this paper,we reported the changes of protein kinase C(PKC)activity in peripheral blood Tlymphocytes and the effect of PKC on T lymphocyte proliferation and apoptosis.We demonstrated that in ITPchildren,the activator(PMA)and inhibitor(H-7)of PKC affected on T lymphocyte proliferation and apoptosisdramatically,but they altered little in healthy children.PKC activity was significantly enhanced in ITP childrentogether with an increased expression of FasL on CD3~+T,CD4~+T and CD8~+T cells,resulting in a positivecorrelation between PKC activity and the expression of FasL on T cells.While the PKC activity and the plateletcount were negatively correlated.Taken together,our findings suggest that the PKC activation may enhance Tlymphocytes activity,suppress T cell apoptosis and be involve in thrombocytes damage as a mechanism related toimmune pathogenesis of ITP.Cellular & Molecular Immunology.2005;2(3):197-203.
It is well-documented that T lymphocyte proliferation and apoptosis are abnormal in idiopathic thrombocytopenic purpura (ITP) children. However, the underlying regulation mechanisms in terms of signal transductionremain unknown. In this paper, we reported the changes of protein kinase C (PKC) activity in peripheral blood Tlymphocytes and the effect of PKC on T lymphocyte proliferation and apoptosis. We demonstrated that in ITPchildren, the activator (PMA) and inhibitor (H-7) of PKC affected on T lymphocyte proliferation and apoptosis diverse, but they altered little in healthy children.PKC activity was significantly enhanced in ITP of childrentogether 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 Tlymphocyte activity, suppress T ce ll apoptosis and be involved in thrombocytes damage as a mechanism related toimmune pathogenesis of ITP. Cellular & Molecular Immunology. 2005; 2 (3): 197-203.