Inhibitory influence of IL-4 on human B cell responsiveness.
- 1 July 1988
- journal article
- research article
- Published by The American Association of Immunologists in The Journal of Immunology
- Vol. 141 (1), 164-173
- https://doi.org/10.4049/jimmunol.141.1.164
Abstract
The role of IL-4 in human B cell activation, proliferation, and differentiation was examined. rIL-2, but not rIL-4, was able to promote maximum proliferation and generation of Ig-secreting cells in cultures of highly purified B cells stimulated with Cowan I Staphylococcus aureus (SA). Addition of rIL-4 to rIL-2-supported cultures of SA-stimulated peripheral blood, spleen, or lymph node B cells dramatically suppressed both proliferation and differentiation. Results from experiments in which rIL-4 was added to culture at progressively later times indicated a requirement for rIL-4 to be present during the first 2 days of a 5-day incubation to cause inhibition of responsiveness. When a two-stage culture system was utilized, rIL-4 was found to support proliferation or differentiation of B cells initially activated with SA for 2 days only minimally. However, rIL-4 did not inhibit responses of SA preactivated B cells supported by IL-2. The presence of rIL-4 during the initial 48-h activation of B cells with SA and rIL-2 resulted in a profound inhibition of the ability of the activated B cells to respond subsequently to rIL-2 or lymphokine-rich T cell supernatants. A similar 48-h incubation with rIL-4 alone without SA had no effect on subsequent B cell responsiveness. The presence of rIFN-gamma during B cell activation decreased the inhibitory effect of IL-4. Other cytokines including IFN-alpha, IL-1, and commercially available low m.w. B cell growth factor also diminished the inhibitory effect of IL-4. These results indicate that IL-4 inhibits the capacity of human B cells to be activated maximally by SA and rIL-2 and therefore suggest a new immunomodulatory role for this cytokine.This publication has 34 references indexed in Scilit:
- Obligatory role of gamma interferon in T cell-replacing factor-dependent, antigen-specific murine B cell responses.The Journal of Experimental Medicine, 1985
- The roles of T cell factors in activation, cell cycle progression, and differentiation of human B cells.The Journal of Immunology, 1985
- Modulation of human natural killer cell function by L-leucine methyl ester: monocyte-dependent depletion from human peripheral blood mononuclear cells.The Journal of Immunology, 1985
- Increased expression of Ia antigens on resting B cells: an additional role for B-cell growth factor.Proceedings of the National Academy of Sciences of the United States of America, 1984
- Interleukin-induced increase in Ia expression by normal mouse B cells.The Journal of Experimental Medicine, 1984
- Differential expression of cell activation markers after stimulation of resting human B lymphocytes.The Journal of Immunology, 1984
- Phenotype of the accessory cell necessary for mitogen-stimulated T and B cell responses in human peripheral blood: delineation by its sensitivity to the lysosomotropic agent, L-leucine methyl ester.The Journal of Immunology, 1983
- Differential sensitivity of human B cell subsets to activation signals delivered by anti-mu antibody and proliferative signals delivered by a monoclonal B cell growth factor.The Journal of Experimental Medicine, 1983
- A monoclonal antibody (anti-Tac) reactive with activated and functionally mature human T cells. I. Production of anti-Tac monoclonal antibody and distribution of Tac (+) cells.The Journal of Immunology, 1981
- Monocyte Dependence of Pokeweed Mitogen-Induced Differentiation of Immunoglobulin-Secreting Cells from Human Peripheral Blood Mononuclear CellsThe Journal of Immunology, 1979