Beyond tumor necrosis factor receptor: TRADD signaling in toll-like receptors

Nien Jung Chen; Iok In Christine Chio; Wen Jye Lin; Gordon Duncan; Hien Chau; David Katz; Huey Lan Huang; Kelly A. Pike; Zhenyue Hao; Yu Wen Su; Kazuo Yamamoto; Renée F. De Pooter; Juan Carlos Zúñiga-Pflücker; Andrew Wakeham; Wen Chen Yeh; Tak W. Mak

doi:10.1073/pnas.0806585105

Beyond tumor necrosis factor receptor: TRADD signaling in toll-like receptors

Nien Jung Chen, Iok In Christine Chio, Wen Jye Lin, Gordon Duncan, Hien Chau, David Katz, Huey Lan Huang, Kelly A. Pike, Zhenyue Hao, Yu Wen Su, Kazuo Yamamoto, Renée F. De Pooter, Juan Carlos Zúñiga-Pflücker, Andrew Wakeham, Wen Chen Yeh, Tak W. Mak

Institute of Microbiology and Immunology

Research output: Contribution to journal › Article › peer-review

97 Scopus citations

Abstract

Tumor necrosis factor receptor 1-associated death domain protein (TRADD) is the core adaptor recruited to TNF receptor 1 (TNFR1) upon TNFα stimulation. In cells from TRADD-deficient mice, TNFα-mediated apoptosis and TNFα-stimulated NF-κB, JNK, and ERK activation are defective. TRADD is also important for germinal center formation, DR3-mediated costimulation of T cells, and TNFα-mediated inflammatory responses in vivo. TRADD deficiency does not enhance IFNγ-induced signaling. Importantly, TRADD has a novel role in TLR3 and TLR4 signaling. TRADD participates in the TLR4 complex formed upon LPS stimulation, and TRADD-deficient macrophages show impaired cytokine production in response to TLR ligands in vitro. Thus, TRADD is a multifunctional protein crucial both for TNFR1 signaling and other signaling pathways relevant to immune responses.

Original language	English
Pages (from-to)	12429-12434
Number of pages	6
Journal	Proceedings of the National Academy of Sciences of the United States of America
Volume	105
Issue number	34
DOIs	https://doi.org/10.1073/pnas.0806585105
State	Published - 26 Aug 2008

Keywords

Innate immunity
TNF

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10.1073/pnas.0806585105

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Chen, N. J., Chio, I. I. C., Lin, W. J., Duncan, G., Chau, H., Katz, D., Huang, H. L., Pike, K. A., Hao, Z., Su, Y. W., Yamamoto, K., De Pooter, R. F., Zúñiga-Pflücker, J. C., Wakeham, A., Yeh, W. C., & Mak, T. W. (2008). Beyond tumor necrosis factor receptor: TRADD signaling in toll-like receptors. Proceedings of the National Academy of Sciences of the United States of America, 105(34), 12429-12434. https://doi.org/10.1073/pnas.0806585105

@article{32517d01f0654cf2a2321238f7b31128,

title = "Beyond tumor necrosis factor receptor: TRADD signaling in toll-like receptors",

abstract = "Tumor necrosis factor receptor 1-associated death domain protein (TRADD) is the core adaptor recruited to TNF receptor 1 (TNFR1) upon TNFα stimulation. In cells from TRADD-deficient mice, TNFα-mediated apoptosis and TNFα-stimulated NF-κB, JNK, and ERK activation are defective. TRADD is also important for germinal center formation, DR3-mediated costimulation of T cells, and TNFα-mediated inflammatory responses in vivo. TRADD deficiency does not enhance IFNγ-induced signaling. Importantly, TRADD has a novel role in TLR3 and TLR4 signaling. TRADD participates in the TLR4 complex formed upon LPS stimulation, and TRADD-deficient macrophages show impaired cytokine production in response to TLR ligands in vitro. Thus, TRADD is a multifunctional protein crucial both for TNFR1 signaling and other signaling pathways relevant to immune responses.",

keywords = "Innate immunity, TNF",

author = "Chen, {Nien Jung} and Chio, {Iok In Christine} and Lin, {Wen Jye} and Gordon Duncan and Hien Chau and David Katz and Huang, {Huey Lan} and Pike, {Kelly A.} and Zhenyue Hao and Su, {Yu Wen} and Kazuo Yamamoto and {De Pooter}, {Ren{\'e}e F.} and Z{\'u}{\~n}iga-Pfl{\"u}cker, {Juan Carlos} and Andrew Wakeham and Yeh, {Wen Chen} and Mak, {Tak W.}",

year = "2008",

month = aug,

day = "26",

doi = "10.1073/pnas.0806585105",

language = "English",

volume = "105",

pages = "12429--12434",

journal = "Proceedings of the National Academy of Sciences of the United States of America",

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Chen, NJ, Chio, IIC, Lin, WJ, Duncan, G, Chau, H, Katz, D, Huang, HL, Pike, KA, Hao, Z, Su, YW, Yamamoto, K, De Pooter, RF, Zúñiga-Pflücker, JC, Wakeham, A, Yeh, WC & Mak, TW 2008, 'Beyond tumor necrosis factor receptor: TRADD signaling in toll-like receptors', Proceedings of the National Academy of Sciences of the United States of America, vol. 105, no. 34, pp. 12429-12434. https://doi.org/10.1073/pnas.0806585105

TY - JOUR

T1 - Beyond tumor necrosis factor receptor

T2 - TRADD signaling in toll-like receptors

AU - Chen, Nien Jung

AU - Chio, Iok In Christine

AU - Lin, Wen Jye

AU - Duncan, Gordon

AU - Chau, Hien

AU - Katz, David

AU - Huang, Huey Lan

AU - Pike, Kelly A.

AU - Hao, Zhenyue

AU - Su, Yu Wen

AU - Yamamoto, Kazuo

AU - De Pooter, Renée F.

AU - Zúñiga-Pflücker, Juan Carlos

AU - Wakeham, Andrew

AU - Yeh, Wen Chen

AU - Mak, Tak W.

PY - 2008/8/26

Y1 - 2008/8/26

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AB - Tumor necrosis factor receptor 1-associated death domain protein (TRADD) is the core adaptor recruited to TNF receptor 1 (TNFR1) upon TNFα stimulation. In cells from TRADD-deficient mice, TNFα-mediated apoptosis and TNFα-stimulated NF-κB, JNK, and ERK activation are defective. TRADD is also important for germinal center formation, DR3-mediated costimulation of T cells, and TNFα-mediated inflammatory responses in vivo. TRADD deficiency does not enhance IFNγ-induced signaling. Importantly, TRADD has a novel role in TLR3 and TLR4 signaling. TRADD participates in the TLR4 complex formed upon LPS stimulation, and TRADD-deficient macrophages show impaired cytokine production in response to TLR ligands in vitro. Thus, TRADD is a multifunctional protein crucial both for TNFR1 signaling and other signaling pathways relevant to immune responses.

KW - Innate immunity

KW - TNF

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JF - Proceedings of the National Academy of Sciences of the United States of America

IS - 34

ER -

Beyond tumor necrosis factor receptor: TRADD signaling in toll-like receptors

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