Essential roles for NF-κB and a Toll/IL-1 receptor domain-specific signal(s) in the induction of IκB-ζ

被引：57

作者：

Eto, A ^{[1
]}

Muta, T ^{[1
]}

Yamazaki, S ^{[1
]}

Takeshige, K ^{[1
]}

机构：

[1] Kyushu Univ, Grad Sch Med Sci, Dept Mol & Cellular Biochem, Fukuoka 8128582, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2003年 / 301卷 / 02期

关键词：

nuclear factor-kappa B; I kappa B-xi; transcriptional induction; toll-like receptor; toll/interleukin-1 receptor domain; innate immunity; macrophage;

D O I：

10.1016/S0006-291X(02)03082-6

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：

IkappaB-zeta a new negative-regulator of nuclear factor-kappaB (NF-kappaB), is strongly induced by lipopolysaccharide or interleukin-1beta stimulation, but not by tumor necrosis factor-alpha. Here, we analyzed the mechanisms for transcriptional induction of IkappaB-zeta. IkappaB-zeta mRNA was induced by overexpression of MyD88 or TRAF6, but not TRAF2. Stimulation of macrophages with peptidoglycan or CpG DNA, which activated Toll-like receptor 2 or 9, respectively, also resulted in IkappaB-zeta induction. Thus, activation of the MyD88-dependent signaling pathway, commonly found downstream of different Toll/interleukin-1 receptor (TIR) domains, is sufficient for IkappaB-zeta induction. The induction was inhibited by treatment with various inhibitors of NF-kappaB activation or by overexpressing IkappaB-alpha or P, indicating essential roles for NF-kappaB in IkappaB-zeta induction. However, overexpression of the NF-kappaB subunits induced IkappaB-alpha, but not IkappaB-zeta. These results indicate the existence of another signal essential for IkappaB-zeta induction, which is specifically mediated by the TIR domain-mediated signaling pathway. (C) 2003 Elsevier Science (USA). All rights reserved.

引用

页码：495 / 501

页数：7

共 33 条

[1] Toll-like receptors in the induction of the innate immune response [J].

Aderem, A ;

Ulevitch, RJ .

NATURE, 2000, 406 (6797) :782-787

[2] Recognition of double-stranded RNA and activation of NF-κB by Toll-like receptor 3 [J].

Alexopoulou, L ;

Holt, AC ;

Medzhitov, R ;

Flavell, RA .

NATURE, 2001, 413 (6857) :732-738

[3] Signaling in plant-microbe interactions [J].

Baker, B ;

Zambryski, P ;

Staskawicz, B ;

DineshKumar, SP .

SCIENCE, 1997, 276 (5313) :726-733

[4] Lipid peroxidation is involved in the activation of NF-kappa B by tumor necrosis factor but not interleukin-1 in the human endothelial cell line ECV304 - Lack of involvement of H2O2 in NF-kappa B activation by either cytokine in both primary and transformed endothelial cells [J].

Bowie, AG ;

Moynagh, PN ;

ONeill, LAJ .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (41) :25941-25950

[5]

Chung JY, 2002, J CELL SCI, V115, P679

[6] Mal (MyD88-adapter-like) is required for Toll-like receptor-4 signal transduction [J].

Fitzgerald, KA ;

Palsson-McDermott, EM ;

Bowie, AG ;

Jefferies, CA ;

Mansell, AS ;

Brady, G ;

Brint, E ;

Dunne, A ;

Gray, P ;

Harte, MT ;

McMurray, D ;

Smith, DE ;

Sims, JE ;

Bird, TA ;

O'Neill, LAJ .

NATURE, 2001, 413 (6851) :78-83

[7] Missing pieces in the NF-κB puzzle [J].

Ghosh, S ;

Karin, M .

CELL, 2002, 109 :S81-S96

[8] A Toll-like receptor recognizes bacterial DNA [J].

Hemmi, H ;

Takeuchi, O ;

Kawai, T ;

Kaisho, T ;

Sato, S ;

Sanjo, H ;

Matsumoto, M ;

Hoshino, K ;

Wagner, H ;

Takeda, K ;

Akira, S .

NATURE, 2000, 408 (6813) :740-745

[9] TIRAP: an adapter molecule in the Toll signaling pathway [J].

Horng, T ;

Barton, GM ;

Medzhitov, R .

NATURE IMMUNOLOGY, 2001, 2 (09) :835-841

[10] TAK1 mediates an activation signal from toll-like receptor(s) to nuclear factor-κB in lipopolysaccharide-stimulated macrophages [J].

Irie, T ;

Muta, T ;

Takeshige, K .

FEBS LETTERS, 2000, 467 (2-3) :160-164

← 1 2 3 4 →