IgE production by normal human lymphocytes is induced by interleukin 4 and suppressed by interferons γ and α and prostaglandin E2

Abstract

The effect of human recombinant interleukin 4 (IL-4) on antibody production by normal peripheral blood mononuclear cells enriched for B cells was investigated. IL-4 preferentially induced IgE synthesis in vitro. In addition, a low induction of IgG production was observed, whereas IL-4 had no effect on IgA and IgM synthesis. The IL-4-induced IgE production by B cells required T cells and monocytes but was specifically inhibited by an anti-IL-4 antiserum indicating that, although IL-4 acts indirectly, it is responsible for the induction of IgE synthesis. Il-4-induced IgE production was blocked in a dose-dependent way by interferon γ (IFN-γ), interferon α (IFN-α), and prostaglandin E2. IFN-γ also inhibited IL-4-induced IgG production. These inhibitory effects of IFN-γ and IFN-α on IgE production cannot be attributed to toxic effects since IFN-α induced IgM production in the presence of IL-4, whereas IFN-γ was ineffective in inhibiting IgG production induced by IL-2. IFN-γ, IFN-α, and prostaglandin E2 also inhibited IL-4-induced expression of the low-affinity receptor for the Fc portion of IgE (CD23) on B cells, indicating that there is an association between CD23 expression and IL-4-induced IgE production. This theory was supported by the finding that IL-4-induced IgE production was inhibited by F(ab')2 fragments of an anti-CD23 monoclonal antibody.