Changes and correlations of T-cell coinhibitory molecule programmed death-1 and interferon-γ in pediatric immune thrombocytopenia

다국어 초록 (Multilingual Abstract)

Background: Immune thrombocytopenia (ITP) is an acquired autoimmune disease characterized by abnormalities of T cells subsets. Programmed death-1 (PD-1) is a co-signaling inhibitory molecule in T cells that is involved in many autoimmune diseases.Purpose: Here we aimed to measure changes in PD-1 expression and serum interferon-γ (IFN-γ) levels before and 1 month after treatment in pediatric patients with newly diagnosed ITP.Methods: We measured PD-1⁺ CD4⁺ T cells percentages using flow cytometry and the serum IFN-γ levels by enzyme-linked immunosorbent assay in 40 pediatric patients with ITP and 20 healthy controls.Results: Compared with healthy controls, the PD-1⁺ CD4⁺ T cells percentages and serum IFN-γ levels were significantly higher in ITP patients before and 1 month after therapy. A correlation study revealed that PD-1⁺ CD4⁺ T cells percentage was negatively associated with platelet count and positively associated with IFN-γ level in patients with ITP. Furthermore, serum IFN-γ levels were significantly decreased in patients after treatment, but no significant change was detected in the percentage of PD-1⁺ CD4⁺ T cells before or 1 month after therapy.Conclusion: PD-1⁺ CD4⁺ T cells expression and IFN-γ levels were increased in patients with ITP. These preliminary data suggest a potential role of PD-1⁺ CD4⁺ T cells as mediators of ITP. We also found a correlation between PD-1⁺ CD4⁺ T cells and both platelet counts and IFN-γ levels. These findings suggest a potential role of PD-1⁺ CD4⁺ T cells and IFN-γ in the pathogenesis of ITP. Further studies investigating PD-1 expression in different T-cell subsets, serum IFN-γ concentrations, and antiplatelet antibodies levels over a longer duration after therapy initiation could delineate the precise role of PD-1 in ITP pathogenesis. Consequently, novel nontraditional therapeutic strategies for ITP patients may become available.