IL-4 potentiates activated T cell apoptosis via an IL-2-dependent-mechanism

被引：31

作者：

Zhang, JA

Bárdos, T

Shao, Q

Tschopp, J

Mikecz, K

Glant, TT

Finnegan, A

机构：

[1] Rush Univ, Rush Presbyterian St Lukes Med Ctr, Dept Orthoped Surg, Sect Biochem & Mol Biol, Chicago, IL 60612 USA

[2] Rush Univ, Rush Presbyterian St Lukes Med Ctr, Dept Internal Med, Chicago, IL 60612 USA

[3] Rush Univ, Rush Presbyterian St Lukes Med Ctr, Dept Immunol Microbiol, Chicago, IL 60612 USA

[4] Rush Univ, Rush Presbyterian St Lukes Med Ctr, Dept Biochem, Chicago, IL 60612 USA

[5] Univ Western Ontario, Dept Anat & Cell Biol, London, ON, Canada

[6] Univ Lausanne, Inst Biochem, CH-1066 Epalinges, Switzerland

来源：

JOURNAL OF IMMUNOLOGY | 2003年 / 170卷 / 07期

关键词：

D O I：

10.4049/jimmunol.170.7.3495

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Activation-induced cell death (AICD) of T cells is one of the major mechanisms of peripheral tolerance. The regulation of AICD by IL-4 is poorly understood. In this study, we report that AICD in IL-4-deficient T cells is significantly reduced compared with that in wild-type T cells. This impaired AICD correlates with the failure to induce degradation of cellular FLIP. IL-4-mediated enhancement of AICD and cellular FLIP degradation requires a Janus kinase/STAT-6 signaling pathway. Unexpectedly, these effects of IL-4 could be blocked by a neutralizing anti-IL-2 Ab, and addition of rIL-2 could completely restore the defective AICD in IL-4-deficient T cells. Furthermore, IL-4 regulates the T cell thresholds for IL-2 signaling during AICD. These data suggest that IL-4 promotes AICD via an IL-2-dependent mechanism.

引用

页码：3495 / 3503

页数：9

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