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

被引：963

作者：

Oshiumi, H

Matsumoto, M

Funami, K

Akazawa, T

Seya, T ^{[1
]}

机构：

[1] Osaka Med Ctr Canc & Cardiovasc Dis, Dept Immunol, Higashinari Ku, Osaka, Japan

[2] Nara Inst Sci & Technol, Dept Mol Immunol, Nara 6310101, Japan

[3] JST, CREST, Tokyo 1000013, Japan

来源：

NATURE IMMUNOLOGY | 2003年 / 4卷 / 02期

关键词：

D O I：

10.1038/ni886

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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.

引用

页码：161 / 167

页数：7

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