Interleukin-18 activates NF-kappa B in murine T helper type 1 cells

被引：171

作者：

Matsumoto, S ^{[1
]}

TsujiTakayama, K ^{[1
]}

Aizawa, Y ^{[1
]}

Koide, K ^{[1
]}

Takeuchi, M ^{[1
]}

Ohta, T ^{[1
]}

Kurimoto, M ^{[1
]}

机构：

[1] HYASHIBARA BIOCHEM LABS INC,FUJISAKI INST,OKAYAMA 702,JAPAN

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 1997年 / 234卷 / 02期

关键词：

D O I：

10.1006/bbrc.1997.6665

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Interleukin-18 (IL-18) activated T helper type 1 (Th1) cells, OVA#4, and induced production of interleukin-2 (IL-2) in costimulation with anti-CD3 antibody. Upon stimulation with IL-18, I kappa B disappeared from cytoplasm and subsequently nuclear factor-kappa B (NF-kappa B) (p65) accumulated in the nucleus. Corresponding with that, DNA binding activity of NF-kappa B (p65 homodimer or p65/p50 heterodimer) was detected in the nucleus. In the transfection experiments, an IL-2 promoter-driven reporter construct showed the similar responsiveness against IL-18 to that of the intrinsic IL-2 gene, and a construct lacking kappa B site failed to respond to IL-18. These results suggest that IL-18 activates NF-kappa B and it is important for enhancement of IL-2 gene expression by Th1 cells stimulated with IL-18. (C) 1997 Academic Press.

引用

页码：454 / 457

页数：4

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