INTERLEUKIN-9 POTENTIATES THE INTERLEUKIN-4-INDUCED IMMUNOGLOBULIN (IGG, IGM AND IGE) PRODUCTION BY NORMAL HUMAN B-LYMPHOCYTES

IgE production by normal peripheral blood lymphocytes (PBL) is known t o be triggered upon stimulation by interleukin (IL)-4. In the present study we showed that IL-9, another T cell-derived cytokine, markedly p otentiated IgE production induced by suboptimal doses of IL-4, whereas no effect of IL-9 was observed in the absence of IL-4.The potentiatin g effect of IL-9 appeared to be associated with the increased frequenc y of IgE-producing cells, as revealed by a specific ELISA-spot assay. Under the same experimental conditions, IL-9 also enhanced the IL-4-in duced IgG production but did not elicit IgM production. However, IL-9 did not amplify the IL-4-dependent expression of membrane-bound and so luble low affinity receptor for IgE (CD23). IL-4-induced IgE productio n was also potentiated by IL-6 but not by tumor necrosis factor-alpha and IL-1beta. The possibility that the activity of IL-9 was mediated b y 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 lymph ocytes co-cultured with irradiated murine EL4 cells. In addition, IL-9 was shown to potentiate the IL-4-induced IgG and IgM production by no rmal human B lymphocytes preactivated with Staphylococcus aureus Cowan strain. Taken together, these data suggest that IL-9 plays a regulato ry role in the IL-4-dependent immunoglobulin production.