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Interleukin-18 expression induced by Epstein-Barr virus-infected cells
1Transplantation Immunology Department, Medicine Branch, Division of Clinical Sciences, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Yaol@mail.nih.gov
Journal of Leukocyte Biology
|May 19, 2001
Summary
Epstein-Barr virus latent membrane protein-1 (LMP-1) induces interleukin-18 (IL-18) expression, which promotes interferon gamma (IFN-gamma) production. This IL-18 pathway contributes to the regression of Burkitt lymphoma tumors.
Area of Science:
- Immunology
- Oncology
- Virology
Background:
- Epstein-Barr virus (EBV)-negative Burkitt lymphomas typically form tumors in mice.
- Tumor regression occurs when EBV-positive cells or EBV latent membrane protein-1 (LMP-1) are introduced.
- Tumor regression involves murine interferon gamma (IFN-gamma) and IFN-gamma-inducible protein-10 (IP-10).
Purpose of the Study:
- To elucidate the mechanisms by which EBV-LMP-1 promotes IFN-gamma expression.
- To investigate the role of interleukin-18 (IL-18) in EBV-mediated Burkitt lymphoma tumor regression.
Main Methods:
- Immunohistochemical analysis of IL-18 and IL-12 expression in regressing and progressing Burkitt tumors.
- Splenocyte cultures treated with EBV-infected cells or LMP-1-transfected cells.
- Neutralizing antibody assays against IL-18 to assess IP-10 expression.
Main Results:
- Murine IL-18 was consistently expressed in regressing Burkitt tumors but not in progressively growing tumors.
- EBV-infected and LMP-1-transfected cells induced IL-18 expression in splenocytes, but not IL-12.
- Neutralizing IL-18 reduced the induction of IP-10 by EBV-immortalized cells.
Conclusions:
- IL-18 is expressed in response to EBV latent proteins.
- IL-18 acts as an endogenous inducer of IFN-gamma expression.
- IL-18 contributes to EBV-mediated Burkitt lymphoma tumor regression.