Topic
TRIF
About: TRIF is a research topic. Over the lifetime, 1287 publications have been published within this topic receiving 95166 citations. The topic is also known as: IIAE6 & MyD88-3.
Papers published on a yearly basis
Papers
TL;DR: It is shown that TRIF is essential for TLR3- and TLR4-mediated signaling pathways facilitating mammalian antiviral host defense and complete loss of nuclear factor kappa B activation in response toTLR4 stimulation is demonstrated.
Abstract: Stimulation of Toll-like receptors (TLRs) triggers activation of a common MyD88-dependent signaling pathway as well as a MyD88-independent pathway that is unique to TLR3 and TLR4 signaling pathways leading to interferon (IFN)-beta production. Here we disrupted the gene encoding a Toll/IL-1 receptor (TIR) domain-containing adaptor, TRIF. TRIF-deficient mice were defective in both TLR3- and TLR4-mediated expression of IFN-beta and activation of IRF-3. Furthermore, inflammatory cytokine production in response to the TLR4 ligand, but not to other TLR ligands, was severely impaired in TRIF-deficient macrophages. Mice deficient in both MyD88 and TRIF showed complete loss of nuclear factor kappa B activation in response to TLR4 stimulation. These findings demonstrate that TRIF is essential for TLR3- and TLR4-mediated signaling pathways facilitating mammalian antiviral host defense.
3,298 citations
TL;DR: Molecules involved in TLR4-mediated signaling are reviewed, including players that are involved in the negative regulation of this important pathway.
3,067 citations
TL;DR: The function of the fifth adaptor, SARM, has been revealed, which negatively regulates TRIF, and it is shown that it acts as a bridging adaptor in the initiation of TLR signalling.
Abstract: Signalling by Toll-like receptors (TLRs) involves five adaptor proteins known as MyD88, MAL, TRIF, TRAM and SARM. Recent insights have revealed additional functions for MyD88 apart from NF-kappaB activation, including activation of the transcription factors IRF1, IRF5 and IRF7, and also a role outside the TLRs in interferon-gamma signalling. Biochemical information on MAL and TRAM has shown that both act as bridging adaptors, with MAL recruiting MyD88 to TLR2 and TLR4, and TRAM recruiting TRIF to TLR4 to allow for IRF3 activation. Finally, the function of the fifth adaptor, SARM, has been revealed, which negatively regulates TRIF. These new insights allow for a detailed description of the function of the five TIR-domain-containing adaptors in the initiation of TLR signalling.
2,760 citations
TL;DR: Toll-like receptors have been established to play an essential role in the activation of innate immunity by recognizing specific patterns of microbial components and TIR domain-containing adaptors provide specificity of TLR signaling.
2,572 citations
TL;DR: It is demonstrated that MyD88 knockout mice lack the ability to respond to LPS as measured by shock response, B cell proliferative response, and secretion of cytokines by macrophages and embryonic fibroblasts, and the inability of MyD 88 knockout mice to induce LPS-dependent gene expression cannot be attributed to lack of the activation of MAP kinases and NF-kappaB.
2,246 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2025 | 16 |
| 2024 | 15 |
| 2023 | 48 |
| 2022 | 100 |
| 2021 | 72 |
| 2020 | 68 |