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It is well known that idiopathic thrombocytopenic purpura (ITP) is an acquired organ-specific autoimmune hemorrhagic disease and dysfunctional cellular immunity is considered important in the pathophysiology of ITP, however, polarization and apoptosis profiles of T lymphocytes remain unclear completely. In this paper, we investigated the polarization of T cell subsets, the expressions of apoptotic proteins Fas/FasL on T cell subsets and the level of antiapoptotic gene bcl-2 and bax mRNA in the bcl-2 family, then discussed the role of them in ITP pathogenesis. We demonstrated that the ratios of Th1/Th2 and Tc1/Tc2 in ITP children increased obviously, the average percentages of Th1 and Th2 also increased clearly, but the average percentages of Tc1 and Tc2 did not changed. In ITP children, the expressions of Fas, FasL on Th, Th1, Th2, Tc, Tc1 and Tc2 increased significantly. The expressions of FasL on Th1 and Tc1 increased sharply vs. Fas, whereas the expressions of Fas on Th2 and Tc2 increased obviously vs. FasL. The expressions of bcl-2 mRNA in ITP children increased significantly, but the expressions of bax mRNA decreased, the ratios of bcl-2/bax mRNA were improved obviously and there were positive correlation between the ratios of Th1/Th2 (IFN- γ+T/IL-4+T) and the ratios of bcl-2/bax mRNA. Taken together, our findings indicate that ITP is Th1 type cell predominant disease although the precise mechanisms await further functional assay. This abnormal polarization of T cell subsets might be related to the high ratios of bcl-2/bax mRNA and the abnormal expressions of Fas, FasL on T cell subsets, as can involve in ITP immunopathogenesis. [ABSTRACT FROM AUTHOR]

Immune thrombocytopenia (ITP) is an acquired autoimmune disease characterized by an immune mediated decrease in platelet number. Disturbance of CD4+ T‐cell homeostasis with simultaneous decrease of CD4+CD25+Foxp3+ regulatory T cells (Tregs) as well as unrestricted proliferation and activation of peripheral CD4+ effector T cells underpin the pathophysiology of ITP. Indirubin is an active ingredient of a traditional Chinese herb called Indigofera tinctoria L. which is clinically used for the treatment of ITP patients. Whether indirubin targets the Tregs/effector T cell‐axis to restore platelet number is unknown. In our in vitro studies, Indirubin could significantly enhance the number and function of Tregs and meanwhile dampen the activation of effector T cells in a dose‐dependent manner. Indirubin was observed to restore the expression of programmed cell‐death 1 (PD1) and phosphatase and tensin homolog (PTEN) on the CD4+ T cells of ITP patients, leading to the subsequent attenuation of the AKT/mTOR pathway. Furthermore, these observations were recapitulated in an active murine model of ITP with a prominent platelet response. Thus, our results identified a potentially novel mechanism of the therapeutic action of indirubin in the treatment of ITP through regulating the homeostasis of CD4+ T cells in a PD1/PTEN/AKT signalling pathway. [ABSTRACT FROM AUTHOR]

To investigate the effect and mechanism of the CD8+ T cells in bone marrow on autologous megakaryocytopoiesis in idiopathic thrombocytopenic purpura (ITP) patients, we prepared bone marrow mononuclear cells (MNCs) from 15 chronic ITP patients and 13 controls. MNCs were cultured in vitro directly (MNC group) or after depleting CD8+ T cells (CD8+ T-dep group) or adding purified autologous CD8+ T cells to CD8+ T-dep MNCs (Coculture group) or adding dexamethasone to the coculture (DEX group) all in semi-solid and liquid culture systems. The quantity and quality of megakaryocytes were measured. The megakaryocyte count was increased in the presence of autologous CD8+ T cells of patients with chronic ITP, while platelet production was reduced. In addition, lower percentages of polyploidy and apoptotic megakaryocytes, and higher levels of soluble Fas (sFas) in supernatant were observed. Dexamethasone successfully corrected this effect of CD8+ T cells on autologous megakaryocytopoiesis. These studies provide evidence that activated CD8+ T cells in bone marrow of patients with chronic ITP might suppress megakaryocyte apoptosis, leading to impaired platelet production. Megakaryocyte apoptosis would be a novel target for the management of ITP. [ABSTRACT FROM AUTHOR]

An introduction is presented in which the editor discusses various reports within the issue that includes significance of Fas pathway among immune thrombocytopenia (ITP) patients; illustration of difference in proportion of several immune cells; and association of ITP with impaired apoptosis.