Interleukin 4 activates human B lymphocytes via transient inositol lipid hydrolysis and delayed cyclic adenosine monophosphate generation

Eur J Immunol. 1990 Jan;20(1):151-6. doi: 10.1002/eji.1830200122.


We report from three independent centers that, in human tonsillar B lymphocytes, human IL4 switches on a series of second messenger changes, the precise sequence of which constitutes a novel signal transduction cascade. It involves an immediate and transient elevation of inositol 1,4,5-trisphosphate and Ca2+ levels. This is followed several minutes later by a sustained rise in cellular cyclic adenosine monophosphate concentration, the triggering of which involves both the Ca2+ rise and an additional, as yet unidentified, IL4-generated signal. Both the products of the initial inositol lipid hydrolysis and the delayed cyclic adenosine monophosphate accumulation are essential for the later induction of CD23 expression, a major phenotypic change promoted in these cells by IL4. The striking contrast between these findings and those that have been observed for the IL4 triggering of murine B cells is discussed.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigens, Differentiation, B-Lymphocyte / analysis
  • B-Lymphocytes / physiology*
  • Calcium / metabolism
  • Cells, Cultured
  • Cyclic AMP / metabolism
  • Diglycerides / metabolism
  • Humans
  • In Vitro Techniques
  • Inositol Phosphates / metabolism
  • Interleukin-4 / pharmacology*
  • Lymphocyte Activation / drug effects*
  • Phosphatidylinositols / metabolism*
  • Receptors, Fc / analysis
  • Receptors, IgE
  • Recombinant Proteins
  • Signal Transduction
  • Time Factors


  • Antigens, Differentiation, B-Lymphocyte
  • Diglycerides
  • Inositol Phosphates
  • Phosphatidylinositols
  • Receptors, Fc
  • Receptors, IgE
  • Recombinant Proteins
  • Interleukin-4
  • Cyclic AMP
  • Calcium