Premium
An IL‐2 receptor β subdomain that controls Bcl‐X L expression and cell survival
Author(s) -
Ciprés Angel,
Gala Salvador,
MartinezA. Carlos,
Mérida Isabel,
Williamson Peter
Publication year - 1999
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/(sici)1521-4141(199904)29:04<1158::aid-immu1158>3.0.co;2-l
Subject(s) - biology , microbiology and biotechnology , receptor , transfection , signal transduction , cell growth , bcl xl , cell cycle , receptor expression , pi3k/akt/mtor pathway , programmed cell death , interleukin 13 receptor , cell , cell culture , apoptosis , insulin like growth factor 1 receptor , growth factor , biochemistry , genetics
Abstract IL‐2 binding to its high‐affinity receptor regulates signaling events that control both lymphocyte cell survival and cell cycle progression. Although many studies have examined the mechanisms by which IL‐2 regulates cell growth, few studies have dissected the pathways involved in promoting cell survival or the coupling of these pathways to the receptor. In the present study, using the pre‐B cell line Baf‐B03 transfected with a truncated form of the IL‐2 receptor (IL‐2R) β chain, we demonstrate that IL‐2‐dependent cell survival requires only the N‐terminal 350 amino acids of the IL‐2Rβ chain. IL‐2‐dependent survival of cells expressing the truncated receptor correlates with increases in receptor‐associated phosphatidylinositol 3‐kinase (PI3K) activity and expression of Bcl‐X L , but not with changes in c‐Myc expression or proliferation. Inhibition of the PI3K pathway in these cells, but not in cells expressing the wild‐type receptor, has a marked effect on the capacity of IL‐2 to prevent cell death and diminishes the Bcl‐X L response. The requirement for IL‐2‐induced PI3K activity in suppressing the onset of apoptotic cell death is discussed.