4.5 Article

Alterations in immune cell subsets and their cytokine secretion profile in childhood idiopathic thrombocytopenic purpura (ITP)

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CLINICAL AND EXPERIMENTAL IMMUNOLOGY
卷 176, 期 2, 页码 291-300

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WILEY
DOI: 10.1111/cei.12279

关键词

Treg; ITP; NK cells; Th1 and Th2 cells

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Immune thrombocytopenic purpura (ITP) is acquired autoimmune disease in children characterized by the breakdown of immune tolerance. This work is designed to explore the contribution of different lymphocyte subsets in acute and chronic ITP children. Imbalance in the T helper type 1 (Th1)/Th2 cytokine secretion profile was investigated. The frequency of T (CD3(+), CD4(+), CD8(+)) and B (CD19(+)) lymphocytes, natural killer (NK) (CD16(+)56(+)) and regulatory T (T-reg) [CD4(+)CD25(+high)forkhead box protein 3 (FoxP3)(+)] cells was investigated by flow cytometry in 35 ITP children (15 acute and 20 chronic) and 10 healthy controls. Plasma levels of Th1 cytokines [interferon (IFN-gamma) and tumour necrosis factor (TNF-alpha)] and Th2 [interleukin (IL)-4, IL-6 and IL-10)] cytokines were measured using enzyme-linked immunosorbent assay (ELISA). The percentage of T-reg (P < 0 center dot 001) and natural killer (NK) (P < 0 center dot 001) cells were significantly decreased in ITP patients compared to healthy controls. A negative correlation was reported between the percentage of T-reg cells and development of acute (r = -0 center dot 737; P < 0 center dot 01) and chronic (r = -0 center dot 515; P < 0 center dot 01) disease. All evaluated cytokines (IFN-gamma, TNF-alpha, IL-4, IL-6 and IL-10) were elevated significantly in ITP patients (P < 0 center dot 001, P < 0 center dot 05, P < 0 center dot 05, P < 0 center dot 05 and P < 0 center dot 001, respectively) compared to controls. In conclusion, our data shed some light on the fundamental role of immune cells and their related cytokines in ITP patients. The loss of tolerance in ITP may contribute to the dysfunction of T-regs. Understanding the role of T cell subsets will permit a better control of autoimmunity through manipulation of their cytokine network.

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