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Cutting edge:: IL-4 induces suppressor of cytokine signaling-3 expression in B cells by a mechanism dependent on activation of p38 MAPK
被引:52
作者:

Canfield, S
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机构: Columbia Univ Coll Phys & Surg, Dept Med, New York, NY 10032 USA

Lee, Y
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机构: Columbia Univ Coll Phys & Surg, Dept Med, New York, NY 10032 USA

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Rothman, P
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机构: Columbia Univ Coll Phys & Surg, Dept Med, New York, NY 10032 USA
机构:
[1] Columbia Univ Coll Phys & Surg, Dept Med, New York, NY 10032 USA
[2] Univ Iowa, Dept Med, Iowa City, IA 52242 USA
关键词:
D O I:
10.4049/jimmunol.174.5.2494
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
The signaling cascade initiated by IL-4 is classically divisible into two major pathways: one mediated by STAT6, and the other by insulin receptor substrates-1 and -2 via activation of PI3K. In murine splenic B cells, the suppressor of cytokine signaling (SOCS)3 is inducible by IL-4 via a mechanism independent of STAT6 and PI3K Sill expression increases 9-fold within 5 h of IL-4 treatment. This induction occurs normally in B cells deficient in STAT6 and is unaffected by pretreatment with the PI3K inhibitor wortmannin, or with the ERK pathway inhibitor, PD98059. However, the IL-4 induction of SOCS3 is blocked by inhibitors of either the JNK or p38 AMPK pathways (SP600125 and SB203580, respectively). Direct examination of these pathways reveals rapid, IL-4-directed activation of p38 MAPK, uncovering a previously unappreciated pathway mediating IL-4 signal transduction.
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页码:2494 / 2498
页数:5
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