Ongoing IgE synthesis by atopic B cells is enhanced by interleukin-3 and suppressed directly by interferon-gamma in vitro.
Human recombinant interleukin-3 (rIL-3; 10 U/ml) consistently augmented spontaneous IgE synthesis by isolated atopic B cells in vitro, whereas rIL-4 (1-1,000 U/ml) failed to induce IgE synthesis by these cells. Recombinant interferon-gamma (rIFN-gamma) suppressed ongoing IgE production by atopic B cells in a dose-dependent manner. IFN-gamma also inhibited IgE synthesis by a human myeloma cell line (U-266), demonstrating the direct effect of IFN-gamma on the terminal differentiation of IgE-secreting plasma cells. IL-3 and IFN-gamma from different sources displayed the same effects on IgE synthesis. Neutralizing antibodies toward IL-3 or IFN-gamma abolished their activities toward IgE synthesis, supporting the specificity of the effect of these cytokines. The quantity of endogenous IFN-gamma produced by stimulated T cells was significantly decreased in atopic patients compared to nonatopic controls, which might be responsible for the propensity of a high blood IgE level in atopic patients.
Department of Child Development, Kumamoto University Medical School, Japan.
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Matsumoto
D001402:B-Lymphocytes / Q000276:immunology*; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000276:immunology*; D007073:Immunoglobulin E / Q000096:biosynthesis*; D007074:Immunoglobulin G / Q000096:biosynthesis; D007371:Interferon-gamma / Q000494:pharmacology*; D007377:Interleukin-3 / Q000494:pharmacology*; D015847:Interleukin-4 / Q000494:pharmacology; D008213:Lymphocyte Activation; D011994:Recombinant Proteins; D013601:T-Lymphocytes / Q000276:immunology; D014407:Tumor Cells, Cultured
D007074:Immunoglobulin G; D007377:Interleukin-3; D011994:Recombinant Proteins; D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma