What question did this study set out to answer?

To identify and characterize novel TIR domain-containing adapter proteins responsible for mediating MyD88-independent Toll-like receptor signaling pathways.

December 1, 2002The Journal of ImmunologyOpen Access

Cutting Edge: A Novel Toll/IL-1 Receptor Domain-Containing Adapter That Preferentially Activates the IFN-β Promoter in the Toll-Like Receptor Signaling

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Authors

MYMasahiro YamamotoKumamoto University SSShintaro SatoKanazawa University KMKiyotoshi MoriKyowa Kirin (Japan)

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Implication

Laboratory study demonstrates that novel adapter TRIF activates interferon-beta and NF-kappaB promoters via TLR3, highlighting a critical mediator of MyD88-independent immune signaling.

Key Points

To identify and characterize novel TIR domain-containing adapter proteins responsible for mediating MyD88-independent Toll-like receptor signaling pathways.
Cloned and characterized TRIF, testing its regulatory activity on NF-kappaB and IFN-beta promoters using overexpression and dominant-negative constructs.
Examined protein-protein interactions between TRIF, Toll-like receptor 3 (TLR3), and the downstream transcription factor interferon regulatory factor 3 (IRF3).
Overexpression of TRIF induced both NF-kappaB-dependent and IFN-beta promoters, an activity distinct from MyD88 and TIRAP which fail to activate the IFN-beta promoter.
Dominant-negative TRIF selectively suppressed TLR3-dependent activation of both NF-kappaB and IFN-beta promoters, as well as TLR2-, TLR4-, and TLR7-mediated NF-kappaB pathways.
Co-immunoprecipitation demonstrated that TRIF physically associates with TLR3 and IRF3, confirming its functional participation in MyD88-independent signaling.

Cite This Study

Yamamoto et al. (2002) studied this question.

synapsesocial.com/papers/6a0f9fa1fa36b6e053fccc5e https://doi.org/10.4049/jimmunol.169.12.6668

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Implication

Laboratory study demonstrates that novel adapter TRIF activates interferon-beta and NF-kappaB promoters via TLR3, highlighting a critical mediator of MyD88-independent immune signaling.

Cutting Edge: A Novel Toll/IL-1 Receptor Domain-Containing Adapter That Preferentially Activates the IFN-β Promoter in the Toll-Like Receptor Signaling

Discussion

Member takes

Implication

Key Points

Cite This Study

Cutting Edge: A Novel Toll/IL-1 Receptor Domain-Containing Adapter That Preferentially Activates the IFN-β Promoter in the Toll-Like Receptor Signaling

Discussion

Member takes

Implication

Key Points

Cite This Study

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