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CYTOKINE PRODUCTION IN RESPONSE TO EPSTEIN-BARR-VIRUS INFECTION OF PERIPHERAL-BLOOD MONONUCLEAR-CELLS IN-VITRO


Whittingham, S; Naselli, G; Harrison, LC; Boyd, AW; Cebon, J; JACK, I
1993-08
IMMUNOLOGY AND CELL BIOLOGY
Journal Article
71
259-264
To obtain a better understanding of the immune response to Epstein-Barr virus (EBV), we measured the cytokines tumour necrosis factor (TNF)-alpha/beta, interleukin-2 (IL-2). interferon-gamma (IFN-gamma), IL-6 and granulocyte-macrophage colony-stimulating factor (GM-CSF) in the conditioned medium of peripheral blood mononuclear cells from 10 healthy adults before and at 48 h and at 1, 2, 3 and 4 weeks following infection in vitro with EBV. Cultures were examined for regression of outgrowths of nascent virus-transformed B cells, and populations of cells in the cultures were analysed by flow cytometry. TNF-alpha/beta was not detected in infected or non-infected cultures. In infected cultures assayed at the nominated times, the highest levels of IL-2 were detected at 48 hours, IFN-gamma at 1 week, IL-6 at 2 weeks and GM-CSF between 2 and 4 weeks. IL-6 and GM-CSF, but not IL-2 or IFN-gamma, were detected in non-infected cultures but at lower levels than in infected cultures. Nine of the 10 healthy adults showed regression of outgrowths of virus-transformed B cells and, of these, seven had antibodies to the EBV capsid antigen (VCA). Strong regression was associated with sequential increases in IL-2, IFN-gamma, and low levels of IL-6 and GM-CSF. Absent or weak regression was associated with an undetectable level of IL-2, a low level of IFN-gamma, high levels of IL-6 and GM-CSF and an increased frequency of cells bearing the phenotype CD20 and HLA-DR in the final weeks of culture. The percentage of cells with a phenotypic marker for natural killer cells remained constant in all cultures over the 4 week period, and there was a modest decrease in the percentage of T cells in both infected and non-infected cultures. The demonstration of different temporal profiles of cytokines is in accord with a programmed cellular immune response to EBV infection which could serve as a model to study the events that modulate the inflammatory response to EBV.
BLACKWELL SCIENCE
TUMOR-NECROSIS-FACTOR; HUMAN B-CELLS; INTERFERON-GAMMA; ETIOLOGICAL AGENT; GROWTH-FACTOR; FACTOR-ALPHA; INTERLEUKIN-1; BETA; INDUCTION; CLONES
10.1038/icb.1993.30
Refer to copyright notice on published article.

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Creation Date 1993-08-01 12:00:00