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Decreased T-cell reactivity to Epstein-Barr virus-infected lymphoblastoid cell lines in multiple sclerosis
  1. Michael Paul Pender (m.hawes{at}
  1. The University of Queensland, Australia
    1. Peter A Csurhes (p.csurhes{at}
    1. The University of Queensland, Australia
      1. Aleksandra Lenarczyk (macky.edmundson{at}
      1. The University of Queensland, Australia
        1. Casey M M Pfluger (c.pfluger{at}
        1. The University of Queensland, Australia
          1. Scott R Burrows (scottb{at}
          1. Queensland Institute of Medical Research, Australia


            Objective: To investigate T-cell and antibody immunity to Epstein–Barr virus (EBV) in multiple sclerosis (MS).

            Methods: Immunoglobulin G (IgG) immunity to EBV nuclear antigen 1 (EBNA1) and viral capsid antigen was measured by enzyme-linked immunosorbent assays, and T-cell immunity was assessed using enzyme-linked immunospot assays to measure the frequency of peripheral blood mononuclear cells (PBMC) producing interferon-gamma in response to autologous EBV-infected B-cell lymphoblastoid cell lines (LCL) in 34 EBV-seropositive healthy subjects and 34 EBV-seropositive MS patients who had not received immunomodulatory therapy in the previous 3 months.

            Results: MS patients had increased levels of anti-EBNA1 IgG but a decreased frequency of LCL-specific T cells, compared to healthy subjects. Using purified populations of CD4+ T cells and CD8+ T cells we showed that the LCL-specific response resides predominantly in the CD8+ population, with a frequency 5–7 fold higher than in the CD4+ population. The decreased CD8+ T-cell response to LCL in MS was not due to decreased HLA class I expression by LCL, and LCL from MS patients could be killed normally by HLA-matched EBV-specific cytotoxic CD8+ T-cell clones from healthy subjects. Furthermore, the decreased CD8+ T-cell immunity to EBV was not due to a primary defect in the function of CD8+ T cells because EBV-specific cytotoxic CD8+ T-cell lines could be generated normally from the PBMC of MS patients.

            Conclusion: This quantitative deficiency in CD8+ T-cell immunity to EBV might be responsible for the accumulation of EBV-infected B cells in the brains of MS patients.

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