INTERLEUKIN-4 ACTIVATES HUMAN LYMPHOCYTES-B VIA TRANSIENT INOSITOL LIPID HYDROLYSIS AND DELAYED CYCLIC ADENOSINE-MONOPHOSPHATE GENERATION

被引:138
作者
FINNEY, M
GUY, GR
MICHELL, RH
GORDON, J
DUGAS, B
RIGLEY, KP
CALLARD, RE
机构
[1] UNIV BIRMINGHAM,SCH MED,DEPT IMMUNOL,BIRMINGHAM B15 2TJ,W MIDLANDS,ENGLAND
[2] UNIV BIRMINGHAM,SCH MED,DEPT BIOCHEM,BIRMINGHAM B15 2TJ,W MIDLANDS,ENGLAND
[3] INST HENRI BEAUFOUR,LES ULIS,FRANCE
[4] INST CHILD HLTH,LONDON WC1N 1EH,ENGLAND
关键词
D O I
10.1002/eji.1830200122
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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. Copyright © 1990 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim
引用
收藏
页码:151 / 156
页数:6
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