Essential Role of Nuclear Factor (NF)-{kappa}B-Inducing Kinase and Inhibitor of {kappa}b (I{kappa}b) Kinase {alpha} in Nf-{kappa}b Activation through Lymphotoxin {beta} Receptor, but Not through Tumor Necrosis Factor Receptor I

doi:10.1084/jem.193.5.631

Published online 5 March 2001.

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© The Rockefeller University Press, 0022-1007/2001/3/631/ $5.00
The Journal of Experimental Medicine, Volume 193, Number 5, March 5, 2001 631-636

Brief Definitive Report

Essential Role of Nuclear Factor (NF)- ${kappa}$ B–Inducing Kinase and Inhibitor of ${kappa}$ b (I ${kappa}$ b) Kinase ${alpha}$ in Nf- ${kappa}$ b Activation through Lymphotoxin β Receptor, but Not through Tumor Necrosis Factor Receptor I

Akemi Matsushima^a, Tsuneyasu Kaisho^b, Paul D. Rennert^c, Hiroyasu Nakano^d, Kyoko Kurosawa^d, Daisuke Uchida^a, Kiyoshi Takeda^b, Shizuo Akira^b, and Mitsuru Matsumoto^a

^a Division of Informative Cytology, Institute for Enzyme Research, University of Tokushima, Tokushima 770-8503, Japan
^b Department of Host Defense, Research Institute for Microbial Diseases, and Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation, Osaka University, Osaka 565-0871, Japan
^c Department of Immunology and Inflammation, Biogen, Incorporated, Cambridge, Massachusetts 02142
^d Department of Immunology and CREST, Japan Science and Technology Corporation, Juntendo University School of Medicine, Tokyo 113-8421, Japan
Division of Informative Cytology, Institute for Enzyme Research, University of Tokushima, 3-18-15 Kuramoto, Tokushima 770-8503, Japan.81-88-633-743481-88-633-7432

mitsuru{at}ier.tokushima-u.ac.jp

Both nuclear factor (NF)- ${kappa}$ B–inducing kinase (NIK) and inhibitorof ${kappa}$ B (I ${kappa}$ B) kinase (IKK) have been implicated as essential componentsfor NF- ${kappa}$ B activation in response to many external stimuli. However,the exact roles of NIK and IKK ${alpha}$ in cytokine signaling still remaincontroversial. With the use of in vivo mouse models, ratherthan with enforced gene-expression systems, we have investigatedthe role of NIK and IKK ${alpha}$ in signaling through the type I tumornecrosis factor (TNF) receptor (TNFR-I) and the lymphotoxinβ receptor (LTβR), a receptor essential for lymphoidorganogenesis. TNF stimulation induced similar levels of phosphorylationand degradation of I ${kappa}$ B ${alpha}$ in embryonic fibroblasts from either wild-typeor NIK-mutant mice. In contrast, LTβR stimulation inducedNF- ${kappa}$ B activation in wild-type mice, but the response was impairedin embryonic fibroblasts from NIK-mutant and IKK ${alpha}$ -deficient mice.Consistent with the essential role of IKK ${alpha}$ in LTβR signaling,we found that development of Peyer's patches was defective inIKK ${alpha}$ -deficient mice. These results demonstrate that both NIKand IKK ${alpha}$ are essential for the induction of NF- ${kappa}$ B through LTβR,whereas the NIK–IKK ${alpha}$ pathway is dispensable in TNFR-I signaling.

Key Words: alymphoplasia • cytokine signaling • I ${kappa}$ B • Akt kinase • Peyer's patch

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