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Epstein–Barr virus and regulatory T cells in Egyptian paediatric patients with acute B lymphoblastic leukaemia
  1. Mohamed E Ateyah1,
  2. Mona E Hashem1,
  3. Mohamed Abdelsalam2
  1. 1Department of Clinical Pathology, Faculty of Medicine, Zagazig University, Zagazig, Sharkia, Egypt
  2. 2Department of Paediatrics, Faculty of Medicine, Zagazig University, Zagazig, Sharkia, Egypt
  1. Correspondence to Dr M E Hashem, Clinical Pathology Department, Zagazig University, Zagazig, Sharkia 23456, Egypt; mm_hashem2001{at}yahoo.com

Abstract

Objective Acute B lymphoblastic leukaemia (B-ALL) is the most common type of childhood malignancy worldwide but little is known of its origin. Recently, many studies showed both a high incidence of Epstein–Barr virus (EBV) infection and high levels of CD4+CD25+Foxp3+(Treg cells) in children with B-ALL. In our study, we investigated the possible relationship between EBV infection and the onset of B-ALL, and its relation to expression of CD4+, CD25high+Foxp3+ T regulatory cells.

Subject and methods We analysed expression and mean fluorescence intensity (MFI) of Treg cells in peripheral blood of 45 children with B-ALL and in 40 apparently healthy children as a control, using flow cytometry. Serum anti-EBV viral capsid antigen (VCA) IgG, anti-EBV nuclear antigen (EBNA) IgG (for latent infection) and anti-EBV VCA IgM (for acute infection) were investigated using ELISA.

Results Analysis of the Treg cells population in patients and controls revealed that expression of CD4+ CD25high+ T lymphocytes was higher in patients than in controls (mean±SD 15.7±4.1 and 10.61±2.6 in patients and controls, respectively, and MFI of Foxp3 was 30.1±7.1 and 16.7±3.7 in patients and controls, respectively (p<0.001)). There was a high incidence of latent EBV infection in patients (31%) compared with controls (10%) while the incidence of acute infection was 12% in patients and 0% in the control group. To study the role of latent EBV infection in the pathogenesis of acute B-ALL, OR was calculated (OR=4.06, coefficient index 1.2–13.6).

Conclusions These findings suggest a possible role for Treg cells and EBV in the pathogenesis of B-ALL. Further studies are needed on the possible mechanisms of tumour genesis related to Treg cells and EBV in children with B-ALL.

  • EBV
  • ALL
  • LEUKAEMIA

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