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J. Biol. Chem., Vol. 278, Issue 50, 49751-49762, December 12, 2003
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*
¶||**¶**
From the
Department of Immunology, Osaka Medical Center for Cancer and Cardiovascular Diseases, Higashinari-ku, Osaka, 537-8511, Japan, the **Department of Molecular Immunology, Nara Institute of Science and Technology, Ikoma, Nara 631-0101, Japan, the Department of Tumor Cell Biology, The Tokyo Metropolitan Institute of Medical Science, 3-18-22 Honkomagome, Bunkyo-ku, Tokyo, 113, Japan, and CREST, Japan Science and Technology Corporation, Tokyo 100-0013, Japan
Lipopolysaccharide (LPS) is an agonist for Toll-like receptor (TLR) 4 and expresses many genes including NF-
B- and interferon regulatory factor (IRF)-3/IFN-inducible genes in macrophages and dendritic cells (DCs). TICAM-1/TRIF was identified as an adapter that facilitates activation of IRF-3 followed by expression of interferon (IFN)-
genes in TLR3 signaling, but TICAM-1 does not directly bind TLR4. Although MyD88 and Mal/TIRAP adapters functions downstream of TLR4, DC maturation and IFN- induction are independent of MyD88 and Mal/TIRAP. In this investigation, we report the identification of a novel adapter, TICAM-2, that physically bridges TLR4 and TICAM-1 and functionally transmits LPS-TLR4 signaling to TICAM-1, which in turn activates IRF-3. In its structural features, TICAM-2 resembled Mal/TIRAP, an adapter that links TLR2/4 and MyD88. However, TICAM-2 per se exhibited minimal ability to activate NF-B and the IFN- promoter. Hence, in LPS signaling TLR4 recruits two types of adapters, TIRAP and TICAM-2, to its cytoplasmic domain that are indirectly connected to two effective adapters, MyD88 and TICAM-1, respectively. We conclude that for LPS-TLR4-mediated activation of IFN-, the adapter complex of TICAM-2 and TICAM-1 plays a crucial role. This results in the construction of MyD88-dependent and -independent pathways separately downstream of the two distinct adapters.
Received for publication, June 3, 2003 , and in revised form, August 19, 2003.
The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EBI Data Bank with accession number(s) AB091054
* This work was supported in part by grants-in-aid from the Ministry of Education, Science, and Culture (Scientific Research on Priority Areas), and the Ministry of Health and Welfare, of Japan. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
The on-line version of this article (available at http://www.jbc.org) contains Annex Figs. 1-3.
¶ Both authors contributed equally to the results of this article.
|| Present address: Dept. of Biology, Graduate School of Science, Osaka University, Toyonaka, Osaka 560-0043, Japan.
To whom correspondence should be addressed: Dept. of Immunology, Osaka Medical Center for Cancer and Cardiovascular Diseases, 1-3-2 Nakamichi, Higashinari-ku, Osaka, 537-8511 Japan. Tel./Fax: 81-6-6973-1209; E-mail: seya-tu{at}mc.pref.osaka.jp.
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