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Interleukin 4 activates human B lymphocytes via transient inositol lipid hydrolysis and delayed cyclic adenosine monophosphate generation
Author(s) -
Finney Michael,
Guy Graeme R.,
Michell Robert H.,
Gordon John,
Dugas Bernard,
Rigley Kevin P.,
Callard Robin E.
Publication year - 1990
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830200122
Subject(s) - inositol , adenosine , second messenger system , cyclic adenosine monophosphate , biology , signal transduction , interleukin 4 , inositol phosphate , microbiology and biotechnology , inositol trisphosphate , medicine , biochemistry , immunology , receptor , cytokine
Abstract 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 Ca 2+ levels. This is followed several minutes later by a sustained rise in cellular cyclic adenosine monophosphate concentration, the triggering of which involves both the Ca 2+ 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.