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Analysis of NF-kappaB activation caused by transient expression of proteins involved in the MyD88-dependent pathway in TLR signaling revealed that AKT1 suppressed signaling that occurs between activation of IKKbeta and that of NF-kappaB.
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TRIF is a downstream protein of TLRs receptors which play a vital role in innate immunity. Expression of TRIF is downregulated in hyperthermia along with inactivation of NF-kappaB pathway.
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These data suggest that IPS-1 plays a more important role than TRIF in the early type I IFN response and that both IPS-1 and TRIF are involved at later stages of Zika virus infection.
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Experiments with homozygous knockouts of Irakm (encoding a suppressor of MyD88 inactivation) and Trif in competitive bone marrow transplants revealed that MyD88 is required for High Fat Diet expansion of granulocyte macrophage progenitors and that Trif is required for pregranulocyte macrophage progenitor expansion.
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Using ovalbumin as model antigen, the authors showed that exposure of dendritic cells to hyperosmolarity strongly inhibits activation of antigen-specific T cells despite enhancement of antigen uptake, processing and presentation. They identified TRIF as key mediator of this phenomenon.
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the present study indicated that MyD88 and TRIF blockades serve notable and equivalent roles in protecting cardiac deterioration from severe sepsis by attenuating cytokine release, reducing neutrophil infiltration and alleviating apoptosis.
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lipopolysaccharide (LPS) application induces proliferation of dormant hematopoietic stem cells (HSC) and impairs HSC self-renewal via TLR4-TRIF-ROS-p38 signaling.
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These results indicate a critical role for Ticam2 in SARS-CoV disease, and highlight the importance of host genetic variation in disease responses.
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Distinct mechanisms downstream of TLR4 signaling mediate myelosuppression and hematopoietic stem cell exhaustion during sepsis through unique effects of MyD88 and TRIF.
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these data show that both Myd88 and TRIF are necessary for Th17 differentiation in the lungs in response to immunization with lipopolysaccharide
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these studies reveal an additional regulatory function of TRIM8 in innate immune responses: TRIM8 catalyzes polyubiquitination of TRIF, resulting in disruption of TRIF-TBK1 interaction
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Stimulation of the TLR4-TRIF pathway can protect against the development of allergic airway disease and that a TRIF-dependent adjuvant effect on CD4(+) ICOS(+) T-cell responses may be a contributing mechanism.
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Monophosphoryl lipid A stimulation of a TLR4-TRIF-PI3K-Akt pathway prevents lipopolysaccharide-induced ERK activation in the medullar thick ascending limb.
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study reporst a key role for TNF/TNFR1 in Yersinia-induced cell death of murine macrophages, which occurs despite the blockade of NF-kappaB and MAPK signaling imposed by Yersinia on infected cells
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STING and TRIF Contribute to Mouse Sepsis, Depending on Severity of the Disease Model
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the role of Toll-like receptor (TLR) 2, TLR4, myeloid differentiation response gene 88, and Toll-IL-1 receptor domain-containing adaptor-inducing interferon-gamma (TRIF), factors critically involved in the TLR signaling pathway, was studied in experimental autoimmune neuritis.
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Juniperus rigida Sieb. extract inhibits macrophage inflammatory responses by attenuating TRIF-dependent signaling and inflammasome activation.
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TRIF-independent pathways can be involved in the downregulation of drug metabolizing enzymes and transporters through TLR4 and 3. JNK-dependent mechanisms likely mediate this downregulation.
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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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TRIF mediates antibacterial defense during Gram-negative pneumonia, at least in part, by inducing IFN-x03B3; at the primary site of infection.
