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Immunomodulating activity in supernatants from EBV immortalized lymphocytes.

B A Blazar, L M Sutton, M Strome

    Cancer Immunology, Immunotherapy : CII
    |January 1, 1986
    PubMed
    Summary

    Epstein-Barr virus (EBV) immortalized B lymphocytes release factors that stimulate T cell responses. These factors may contribute to B lymphocyte transformation by EBV.

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    Area of Science:

    • Immunology
    • Virology
    • Cell Biology

    Background:

    • Epstein-Barr virus (EBV) immortalized B lymphocytes exhibit an autostimulatory cycle.
    • These B cells release soluble factors that influence immune cell activity.

    Purpose of the Study:

    • To investigate the nature of soluble factors released by EBV-immortalized B cells.
    • To determine the effect of these factors on T cell responses and B cell proliferation.

    Main Methods:

    • Culturing EBV-immortalized B lymphocyte lines.
    • Analyzing culture supernatants (Growth Enhancing media) for biological activity.
    • Assessing the impact of GE media on Concanavalin A (Con A) stimulated human mononuclear cells.
    • Evaluating effects on purified B cells stimulated with pokeweed mitogen (PWM).
    • Testing IL-2 dependent cell growth.
    • Measuring IL-1 activity using mouse thymocyte assays.

    Main Results:

    • GE media modulated Con A responses biphasically: stimulation at low concentrations, inhibition at high concentrations.
    • Stimulatory concentrations of GE media enhanced and accelerated the blastogenic response to Con A.
    • GE media reduced the response of purified B cells to PWM.
    • GE media did not support IL-2 dependent cell growth.
    • Some EBV-carrying B cell lines produced IL-1-like activity in mouse thymocyte assays.
    • LPS-stimulated B cell lines also showed IL-1-like effects.

    Conclusions:

    • EBV-immortalized B cells may produce IL-1-like factors that cooperate in T cell responses.
    • These factors could play a role in EBV-mediated B lymphocyte transformation.
    • The study highlights a potential mechanism for immune dysregulation in EBV infections.

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