Involvement of levels of Toll like receptor-4 in monocytes, CD4 + T-lymphocyte subsets, and cytokines in patients with immune thrombocytopenic purpura

摘要

Introduction Toll-like receptors have been found to be associated with immune-mediated diseases but it is still not clear whether they play a role in immune thrombocytopenic purpura (ITP), especially TLR4. CD4 + T-lymphocyte abnormalities, including Th17, Th1, Th2, and regulator T cell (Treg), are considered important in ITP. There have been few studies regarding the expression of TLR4 and the relationships between TLR4 and Th17 levels in ITP. Materials and Methods In this study, we evaluated the expression of TLR4 in monocytes, the plasma concentrations of IL-23, IL-17 and the profiles of Th17, Th1, Th2 cells in 70 patients with ITP and 31 healthy controls. In addition, we evaluated IL-2 and Treg cells in 46 cases of 70 patients with ITP and the same 31 controls. Results Higher levels of TLR4 expression, higher relative numbers of Th17 and Th1 cells and lower levels of Treg cells were observed in patients when compared with controls (p = 0.001 for TLR4; p 0.001 for Th17; p = 0.014 for Th1; p = 0.001 for Treg). The levels of IL-23 and IL-2 were increased (p = 0.022 for IL-23; p = 0.025 for IL-2), the relative levels of Th2 and concentrations of IL-17 were similar across both groups (p = 0.446 for Th2; p = 0.316 for IL-17). A significant negative correlation was observed between levels of TLR4 and Treg(r = -0.544, p 0.001), but a significantly positive correlation was observed between IL-2 and IL-23 concentration in patients (r = 0.441, p = 0.004). Neither the correlation between TLR4 and the other CD4 + T cells and cytokines nor the correlation between the three cytokines and CD4+ T cells was found to be statistically significant. Conclusions Our data showed that TLR4, CD4 + T cells (Th1, Th17 and Treg cells) and related cytokines (IL-23, IL-2) may take part in the pathogenesis of ITP. TLR4 may play a role through the TLR4-cytokine-CD4+ T lymphocyte cell pathway.