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Article
Nature Immunology  4, 161 - 167 (2003)
Published online: 21 January 2003; | doi:10.1038/ni886

TICAM-1, an adaptor molecule that participates in Toll-like receptor 3−mediated interferon-bold beta induction

Hiroyuki Oshiumi1, 3, Misako Matsumoto1, 3, Kenji Funami1, 2, Takashi Akazawa1 & Tsukasa Seya1, 2, 3

1  Department of Immunology, Osaka Medical Center for Cancer and Cardiovascular Diseases, Higashinari-ku, Osaka, Japan.

2  Department of Molecular Immunology, Nara Institute of Science and Technology, Ikoma, Nara 631-0101, Japan.

3  CREST, JST (Japan Science and Technology Corporation), Tokyo 100-0013, Japan.

 H.O. and M.M. contributed equally to this work.

Correspondence should be addressed to Tsukasa Seya seya-tu@mc.pref.osaka.jp
Human Toll-like receptor (TLR) 3 recognizes double-stranded (ds) RNA and induces production of interferon (IFN)-beta independent of the adaptor molecules MyD88 and TIRAP. Thus, another adaptor must exist that preferentially mediates TLR3-dependent production of IFN-beta. We have identified an alternative adaptor, designated Toll-interleukin 1 receptor domain (TIR)-containing adaptor molecule (TICAM)-1, that can physically bind the TIR domain of TLR3 and activate the IFN-beta promoter in response to poly(I):poly(C). Thus, dsRNA-TLR3−dependent production of IFN-beta is mediated mainly by TICAM-1. This TICAM-1−dependent pathway may have a role in other TLR−IFN-beta pathways, which form part of the MyD88-independent cellular immune response.

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Nature Immunology
ISSN: 1529-2908
EISSN: 1529-2916
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