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Findings confirm that signalling through MyD88 is the primary driver for Lipopolysaccharide-dependent NF-kappaB translocation to the nucleus. The pattern of NF-kappaB dynamics in TRIF-deficient cells does not, however, directly reflect the kinetics of TNFalpha promoter activation, supporting the concept that TRIF-dependent signalling plays an important role in the transcription of this cytokine.
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STING-mediated innate immune responses and dendritic cell maturation do not require TICAM-1 in myeloid lineage immune cells.
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Mice with myeloid cell specific TIR-domain-containing adapter-inducing interferon-beta (TRIF) knockout showed a trend towards accelerated onset of STZ-induced diabetes, while TRIF deficiency resulted in reduced IDO expression in vivo and in vitro. MyD88 signaling in myeloid cells is a critical pathogenic factor in autoimmune diabetes, which is antagonized by TRIF-dependent responses.
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Findings suggest that Toll/IL-1R domain-containing adapter-inducing IFN-beta may be involved in the epileptogenesis of temporal lobe epilepsy, which would make it a potential therapeutic target for the treatment of epilepsy.
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The TLR3/TICAM-1 pathway inhibits polyposis through suppression of c-Myc expression and supports long survival in Apc (Min/+) mice.
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Versican is produced by Trif- and type I interferon-dependent signaling in macrophages and contributes to fine control of innate immunity in lungs
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TRIF contributes to murine host defense during the initial response to leptospiral infection
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work reveals that simulated microgravity promotes the apoptotic response through a combined modulation of the Uev1A/TICAM/TRAF/NF-kappaB-regulated apoptosis and the p53/PCNA- and ATM/ATR-Chk1/2-controlled DNA-damage response pathways.
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Results show that Monophosphoryl lipid A-induced neutrophil and monocyte recruitment, expansion of bone marrow progenitors and augmentation of neutrophil adhesion molecule expression are regulated by both the MyD88- and TRIF-dependent pathways.
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TRIF and STING interacted directly, through their carboxy-terminal domains, to promote STING dimerization, intermembrane translocation, and signaling.
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Upon stimulation with poly(I:C), malaria parasite-infected red blood cells (iRBCs), or vesicular stomatitis virus (VSV), FOSL1 "translocated" from the nucleus to the cytoplasm, where it inhibited the interactions between TNF receptor-associated factor 3 (TRAF3), TIR domain-containing adapter inducing IFN-beta (TRIF), and Tank-binding kinase 1 (TBK1) via impairing K63-linked polyubiquitination of TRAF3 and TRIF.
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These results suggested the importance of TRIF in TLR2 mediated foam cell formation via inflammatory mediators, including MCP-1.
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DENV replication and IFNalpha/beta, TNF-alpha, IL-12 and IL-18 in infected cultures at 24h were found. All of these parameters were significantly decreased after TRIF, MYD88 or NF-kB inhibition
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The authors demonstrate that, in addition to MyD88, Yersinia pseudotuberculosis inhibits TRIF signaling through the type III secretion system effector YopJ.
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Results show that toll/IL-1 domain-containing adaptor inducing IFN-beta (TRIF) is essential for Toll-like receptors TLR3- and TLR4-mediated innate immune responses in peritoneal mesothelial cells (PMCs).
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Data show that annexin A2 (AnxA2) directly exerted negative regulation of inflammatory responses through Toll-like receptor 4 (TLR4)-initiated TRAM protein-TRIF protein pathway occurring on endosomes.
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ProTalpha preconditioning-induced prevention of retinal ischemic damage is mediated by selective activation of the TIR-domain-containing adapter-inducing interferon-beta interferon regulatory factor 3 pathway downstream of toll-like receptor 4 in microglia
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signaling through TRIF is important for the inflammatory response of AngII-induced abdominal aortic aneurysm formation
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analysis of how MyD88 and TRIF affect TLR4 activation
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In mice with nonfunctional TRIF (Trif(mut) mice), Ang II-induced hypertension and cardiac hypertrophy were abrogated, and proinflammatory gene expression in heart and kidneys was unchanged or decreased. These results indicate that Ang II induces activation of a proinflammatory innate immune response, causing hypertension and cardiac hypertrophy, which require functional adaptor protein TRIF-mediated pathways.
