Research progress of peripheral blood regulatory T cell/helper T cell 17 imbalance and relevant gene methylation in immune thrombocytopenia

Abstract

Immune thrombocytopenia (ITP) is an autoimmune hemorrhagic disease. The classic pathogenesis of ITP is that the production of autoantibodies against platelet membrane glycoproteins, which mediates platelet destruction. In recent years, it has been found that there are still many other mechanisms in ITP inducing thrombocytopenia and platelet damage, among which abnormal cellular immunity plays an important role. In cellular immunity, CD4+ CD25high CD127- regulatory T cells (Treg) are a group of T cell subsets that exist in human peripheral blood and spleen and can inhibit auto-reactive T cell responses; T helper cells (Th)17 is a newly discovered T cell subset that secretes interleukin (IL)-17, involved in mediating inflammatory response, which is of great significance in autoimmune diseases. Several studies showed that Treg/Th17 imbalance and abnormal expression of specific transcription factors folkhead box protein (Foxp)3 and retinoic acid-related orphan nuclear receptor (ROR)-γt were observed in peripheral blood of ITP patients. DNA methylation induces Foxp3 gene silencing and abnormal activation of IL-6/STAT3 signaling pathway, which may be the mechanism leading to Treg/Th17 imbalance and causes of ITP. The proposed demethylation treatment may provide new ideas for the molecular targeted treatment of ITP, but its scientificity, effectiveness and safety still need to be confirmed by further studies. The author reviews literature on the role of Treg/Th17 imbalance and relevant gene methylation mechanism in the occurrence, development and treatment of ITP. Key words: T-lymphocytes, regulatory; T-lymphocyte subsets; DNA methylation; Thrombocytopenia; Helper T lymphocyte 17; Decitabine