Effect of protein kinase C on T lymphocyte proliferation and apoptosis in acute idiopathic thrombocytopenic purpura.

Previous studies have shown that T lymphocyte proliferation and apoptosis are abnormal in idiopathic thrombocytopenic purpura (ITP) children; however, the underlying regulated mechanisms in signal transductions remain unknown. In this paper, we investigated the changes of protein kinase C (PKC) activity in peripheral blood T lymphocytes and the effect of PKC on the peripheral blood T lymphocyte proliferation and apoptosis in ITP children. We demonstrated that T lymphocytes from ITP children were more susceptible to the activator (phorbol myristate acetate) and the inhibitor (H-7) of PKC. In ITP children, phorbol myristate acetate and H-7 dramatically affected T lymphocyte proliferation and apoptosis, but altered little in healthy children. Compared with healthy children, PKC activity was significantly enhanced in ITP children, increasing the expressions of Fas ligand on CD3+, CD4+ and CD8+ T cells, indicating positive correlations between PKC activity and the expressions of Fas ligand on T cells, while the relations between PKC activity and platelet count showed negative correlations. Taken together, our findings suggest that PKC signal transductions may participate in the procedure of T lymphocyte proliferation and apoptosis in ITP children. PKC activation may enhance T lymphocyte activity, suppress T cell apoptosis, and be involved in thrombocyte damage, which can be related to the immunity pathogenesis of ITP.