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

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Abstract

Summary: 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 (Treg) [CD4+CD25+highforkhead 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-γ) and tumour necrosis factor (TNF-α)] and Th2 [interleukin (IL)-4, IL-6 and IL-10)] cytokines were measured using enzyme-linked immunosorbent assay (ELISA). The percentage of Treg (P<0·001) and natural killer (NK) (P<0·001) cells were significantly decreased in ITP patients compared to healthy controls. A negative correlation was reported between the percentage of Treg cells and development of acute (r=-0·737; P<0·01) and chronic (r=-0·515; P<0·01) disease. All evaluated cytokines (IFN-γ, TNF-α, IL-4, IL-6 and IL-10) were elevated significantly in ITP patients (P<0·001, P<0·05, P<0·05, P<0·05 and P<0·001, 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 Tregs. Understanding the role of T cell subsets will permit a better control of autoimmunity through manipulation of their cytokine network. © 2014 British Society for Immunology.

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Talaat, R. M., Elmaghraby, A. M., Barakat, S. S., & El-Shahat, M. (2014). Alterations in immune cell subsets and their cytokine secretion profile in childhood idiopathic thrombocytopenic purpura (ITP). Clinical and Experimental Immunology, 176(2), 291–300. https://doi.org/10.1111/cei.12279

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