IgE production by normal human lymphocytes is induced by interleukin 4 and suppressed by interferons gamma and alpha and prostaglandin E2.

DOI Web Site 52 Citations
  • J Pène
    UNICET, Laboratory for Immunological Research, Dardilly, France.
  • F Rousset
    UNICET, Laboratory for Immunological Research, Dardilly, France.
  • F Brière
    UNICET, Laboratory for Immunological Research, Dardilly, France.
  • I Chrétien
    UNICET, Laboratory for Immunological Research, Dardilly, France.
  • J Y Bonnefoy
    UNICET, Laboratory for Immunological Research, Dardilly, France.
  • H Spits
    UNICET, Laboratory for Immunological Research, Dardilly, France.
  • T Yokota
    UNICET, Laboratory for Immunological Research, Dardilly, France.
  • N Arai
    UNICET, Laboratory for Immunological Research, Dardilly, France.
  • K Arai
    UNICET, Laboratory for Immunological Research, Dardilly, France.
  • J Banchereau
    UNICET, Laboratory for Immunological Research, Dardilly, France.

Abstract

<jats:p>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 gamma (IFN-gamma), interferon alpha (IFN-alpha), and prostaglandin E2. IFN-gamma also inhibited IL-4-induced IgG production. These inhibitory effects of IFN-gamma and IFN-alpha on IgE production cannot be attributed to toxic effects since IFN-alpha induced IgM production in the presence of IL-4, whereas IFN-gamma was ineffective in inhibiting IgG production induced by IL-2. IFN-gamma, IFN-alpha, 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.</jats:p>

Journal

Citations (52)*help

See more

Keywords

Details 詳細情報について

Report a problem

Back to top