Cutting edge: a novel Toll/IL-1 receptor domain-containing adapter that preferentially activates the IFN-β promoter in the Toll-like receptor signaling

M Yamamoto, S Sato, K Mori, K Hoshino… - The Journal of …, 2002 - journals.aai.org
M Yamamoto, S Sato, K Mori, K Hoshino, O Takeuchi, K Takeda, S Akira
The Journal of Immunology, 2002journals.aai.org
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 …
Abstract
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-β (TRIF). As is the case in MyD88 and TIRAP, overexpression of TRIF activated the NF-κB-dependent promoter. A dominant-negative form of TRIF inhibited TLR2-, TLR4-, and TLR7-dependent NF-κB activation. Furthermore, TRIF, but neither MyD88 nor TIRAP, activated the IFN-β promoter. Dominant-negative TRIF inhibited TLR3-dependent activation of both the NF-κB-dependent and IFN-β 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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