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Cutting Edge |
Promoter in the Toll-Like Receptor Signaling1
Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, and Solution Oriented Research for Science and Technology, Japan Science and Technology Corporation, Suita, Osaka, Japan
MyD88 is a Toll/IL-1 receptor (TIR) domain-containing
adapter common to signaling pathways via Toll-like receptor (TLR)
family. However, accumulating evidence demonstrates the existence of a
MyD88-independent pathway, which may explain unique biological
responses of individual TLRs, particularly TLR3 and TLR4. TIR
domain-containing adapter protein (TIRAP)/MyD88 adapter-like, a
second adapter harboring the TIR domain, is essential for
MyD88-dependent TLR2 and TLR4 signaling pathways, but not for
MyD88-independent pathways. Here, we identified a novel TIR
domain-containing molecule, named TIR domain-containing adapter
inducing IFN-
(TRIF). As is the case in MyD88 and TIRAP,
overexpression of TRIF activated the NF-
B-dependent promoter.
A dominant-negative form of TRIF inhibited TLR2-, TLR4-, and
TLR7-dependent NF-B activation. Furthermore, TRIF, but neither MyD88
nor TIRAP, activated the IFN- promoter. Dominant-negative TRIF
inhibited TLR3-dependent activation of both the NF-B-dependent and
IFN- promoters. TRIF associated with TLR3 and IFN regulatory factor
3. These findings suggest that TRIF is involved in the TLR signaling,
particularly in the MyD88-independent pathway.
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