-
Together, our findings demonstrate that TRIF signaling is required for caspase-11-dependent immune responses and lethality in endotoxemia and sepsis, and provide novel mechanistic insights into how LPS induces caspase-11 activation during bacterial infection.
-
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.
-
STING-mediated innate immune responses and dendritic cell maturation do not require TICAM-1 in myeloid lineage immune cells.
-
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.
-
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.
-
The TLR3/TICAM-1 pathway inhibits polyposis through suppression of c-Myc expression and supports long survival in Apc (Min/+) mice.
-
Versican is produced by Trif- and type I interferon-dependent signaling in macrophages and contributes to fine control of innate immunity in lungs
-
TRIF contributes to murine host defense during the initial response to leptospiral infection
-
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.
-
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.
-
TRIF and STING interacted directly, through their carboxy-terminal domains, to promote STING dimerization, intermembrane translocation, and signaling.
-
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.
-
These results suggested the importance of TRIF in TLR2 mediated foam cell formation via inflammatory mediators, including MCP-1.
-
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
-
The authors demonstrate that, in addition to MyD88, Yersinia pseudotuberculosis inhibits TRIF signaling through the type III secretion system effector YopJ.
-
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).
-
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.
-
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
-
signaling through TRIF is important for the inflammatory response of AngII-induced abdominal aortic aneurysm formation
-
analysis of how MyD88 and TRIF affect TLR4 activation
