Interleukin‐9 potentiates the interleukin‐4‐induced immunoglobulin (IgG, IgM and IgE) production by normal human B lymphocytes

Abstract

IgE production by normal peripheral blood lymphocytes (PBL) is known to be triggered upon stimulation by interleukin (IL)‐4. In the present study we showed that IL‐9, another T cell‐derived cytokine, markedly potentiated IgE production induced by suboptimal doses of IL‐4, whereas no effect of IL‐9 was observed in the absence of IL‐4. The potentiating effect of IL‐9 appeared to be associated with the increased frequency of IgE‐producing cells, as revealed by a specific ELISA‐spot assay. Under the same experimental conditions, IL‐9 also enhanced the IL‐4‐induced IgG production but did not elicit IgM production. However, IL‐9 did not amplify the IL‐4‐dependent expression of membrane‐bound and soluble low affinity receptor for IgE (CD23). IL‐4‐induced IgE production was also potentiated by IL‐6 but not by tumor necrosis factor‐α and IL‐β The possibility that the activity of IL‐9 was mediated by IL‐6 released from accessory cells was excluded by the observations that monocyte depletion did not abolish the effect of IL‐9 and that IL‐9 was still active on fluorescence assisted cell sorted CD20⁺ B lymphocytes co‐cultured with irradiated murine EL4 cells. In addition, IL‐9 was shown to potentiate the IL‐4‐induced IgG and IgM production by normal human B lymphocytes preactivated with Staphylococcus aureus Cowan strain. Taken together, these data suggest that IL‐9 plays a regulatory role in the IL‐4‐dependent immunoglobulin production.