Abstract
Immune thrombocytopenia (ITP) is a disease characterized by isolated thrombocytopenia. Abnormal effector T cell activation is an important mechanism in the pathogenesis of ITP. Regulatory T cells (Treg) have a strong immunosuppressive function for T cell activation and their importance in the pathophysiology and clinical treatment of ITP has been confirmed. Myeloid-derived suppressor cells (MDSCs) are other immunosuppressive cells, which can also suppress T cell activation by secreting arginase, iNOS and ROS, and are essential for Treg cells’ differentiation and maturation. Therefore, we speculate that MDSCs might also be involved in the immune-dysregulation mechanism of ITP. In this study, we tested MDSCs and Treg cells in peripheral blood samples of twenty-five ITP patients and ten healthy donors. We found that MDSCs and Treg cells decreased simultaneously in active ITP patients. Relapsed ITP patients showed lower MDSCs levels compared with new patients. All patients received immunosuppressive treatment including dexamethasone alone or in combination with intravenous immune globulin. We found that MDSCs’ level after treatment correlated with platelet recovery. Our study is the first that focused on MDSCs’ role in ITP. Based on our results, we concluded that circulating MDSCs could predict disease activity and treatment response in ITP patients. This preliminary conclusion indicates a substantial significance of MDSCs in the pathophysiology and clinical treatment of ITP, which deserves further investigation.
Highlights
Immune thrombocytopenia (ITP) is an acquired immunemediated disease characterized by isolated thrombocytopenia, and is characterized by increased platelet destruction that is mediated by autoantibodies
intravenous immunoglobulin (IVIg) application did not promote Myeloid-derived suppressor cells (MDSCs) or Treg cell recovery after treatment. This result indicates that MDSCs and Treg cells could be markers for ITP disease activity, while immunosuppressive treatment helps restore the amount of MDSCs and Treg cells in ITP patients
Treg cell deficiency was reported as a marker for the disease activity of ITP
Summary
Immune thrombocytopenia (ITP) is an acquired immunemediated disease characterized by isolated thrombocytopenia, and is characterized by increased platelet destruction that is mediated by autoantibodies. Abnormal T cell activation has recently become regarded as a more important mechanism in the pathogenesis of ITP [1,2]. Regulatory T cells (Treg) are characterized as CD4+/FoxP3+ and suppress abnormal T cell activation by secreting TGF-b, IL-10, and IL-4 (among others), thereby inducing immune tolerance [3]. Accumulating data have confirmed the importance of Treg cells in the pathophysiology and clinical treatment of ITP [4,5,6,7]. Conventional treatments for ITP include high-dose dexamethasone (DXM), intravenous immunoglobulin (IVIg) and other immune-suppressive regimens [8,9,10]. High-dose DXM treatment could expand regulatory T cells in ITP patients, suppressing the abnormal T cell activation [11]
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