Imbalance of T Lymphocyte Subsets in Adult Immune Thrombocytopenia.

Abstract

BackgroundPrimary immune thrombocytopenia (ITP) is defined as an acquired autoimmune disease characterized by isolated thrombocytopenia. This work is to further clarify the relationship between T cell immune dysfunction and the pathogenesis of ITP.Methods37 adult patients with ITP were selected and were classified into newly diagnosed ITP (nITP, n = 13), persistent ITP (pITP, n = 6) and chronic ITP (cITP n = 18). The frequency of cytotoxic T lymphocytes (Tc1, Tc2, and Tc17) and helper T cells (Th1, Th2, and Th17), Tregs, and the expression of chemokine receptors and PD-1 on CD4+ T cells were investigated by flow cytometry. Plasma levels of T cell-related cytokines (IL-2, IL-4, IL-6, IL-10, TNF-α, IFN-γ, IL-17) were measured by cytometric beads array (CBA).ResultsThe percentage of Tc1 in cITP was greatly higher than nITP and healthy controls (p < 0.05, p < 0.01). The percentage of Treg in nITP and cITP groups was remarkably lower than those in healthy control group (p < 0.05, p < 0.001); and according to platelet count analysis (PLT<50x109/L or PLT>50x109/L), Treg cells in ITP group were significantly lower than those in healthy control group (p < 0.001, p < 0.05). The percentage of CD4+CXCR3+ of cITP was significantly higher than healthy controls and nITP (p < 0.01, p < 0.05). The percentage of CD4+CCR6+ in cITP was significantly higher than healthy controls and nITP (p < 0.001, p < 0.05). The expression of PD-1 in cITP patients was higher than healthy control (p < 0.05), but there was no significant difference among nITP, pITP and cITP (p = 0.25). The levels of IL-2, IFN-γ and TNFα in nITP group and cITP group were significantly higher than those in healthy control group (p < 0.01, p < 0.05; p < 0.01, p < 0.05; p < 0.05, p < 0.05), and the level of IL-10 in nITP group was significantly higher than that in pITP group (p < 0.05).ConclusionOur results suggest that T lymphocyte immune dysfunction does exist in adult ITP patients and plays an important role in the pathogenesis of ITP.