|
Hepatitis C
|
0.090 |
Biomarker
|
disease |
BEFREE |
In conclusion, our work revealed a new mechanism for HCV to evade innate immune response by blocking the TLR3-mediated interferon signaling via NS4B-induced TRIF degradation.
|
29782532 |
2018 |
|
Hepatitis C
|
0.090 |
Biomarker
|
disease |
BEFREE |
The activity of asunaprevir-regulated innate immunity signal pathway was assessed with IFN-β promoter or IFN-stimulated responsive element (ISRE) reporter assays and immunoblotting of key signal proteins. siRNA-mediated MAVS and TRIF knockdown of cells was performed to assess the effect of asunaprevir-regulated innate immunity against HCV and DENV.
|
28473813 |
2017 |
|
Hepatitis C
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
In addition, mouse CD8+ DCs mature in response to HCV-infected hepatocytes unless the TLR3/TICAM-1 pathway is blocked.
|
26512676 |
2015 |
|
Hepatitis C
|
0.090 |
Biomarker
|
disease |
BEFREE |
Recent studies established the essential role of TLR3-TICAM-1 pathway in type III IFN production in response to HCV infection.
|
24532585 |
2014 |
|
Hepatitis C
|
0.090 |
Biomarker
|
disease |
BEFREE |
HCV-encoded NS3/4A protease plays an important role in HCV immune evasion by cleaving key adapter proteins VISA and TRIF of the RIG-I-like receptors and Toll-like receptors mediated interferon (IFN) induction pathways.
|
23137809 |
2013 |
|
Hepatitis C
|
0.090 |
Biomarker
|
disease |
BEFREE |
Although HCV genomic RNA contains pathogen-associated molecular pattern (PAMP) that is able to induce host interferon responses, HCV can shut down the responses by using the viral NS3/4A protease to cleave MAVS/VISA and TRIF, two key adaptor molecules essential for the interferon signaling activation.
|
23542348 |
2013 |
|
Hepatitis C
|
0.090 |
Biomarker
|
disease |
BEFREE |
The HCV NS3/4A protease efficiently cleaves and inactivates two important signaling molecules in the sensory pathways that react to HCV pathogen-associated molecular patterns (PAMPs) to induce interferons (IFNs), i.e., mitochondrial antiviral signaling protein (MAVS) and Toll-IL-1 receptor domain-containing adaptor inducing IFN-β (TRIF).
|
23063572 |
2013 |
|
Hepatitis C
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
NS3/4A protease inhibition can prevent Cardif and/or TRIF inactivation during HCV infection, thereby maintaining the innate immune response.
|
18037183 |
2008 |
|
Pancreatitis
|
0.020 |
Biomarker
|
disease |
BEFREE |
In comparison to wildtype and Ticam1 KO mice, Tlr3 KO mice exhibited the highest severity of pancreatitis with an increased NF-κB activation and elevated expression of the pro-inflammatory cytokines Il6 and Tnf, although the amount of infiltrating immune cells was unaffected.
|
30583980 |
2019 |
|
Septicemia
|
0.020 |
Biomarker
|
disease |
BEFREE |
These protective effects were mediated through MPLA stimulation of a Toll/IL-1 receptor domain-containing adaptor-inducing IFN-β-(TRIF)-dependent phosphatidylinositol 3-kinase-Akt pathway that prevents sepsis- and LPS-induced ERK activation.
|
29741098 |
2018 |
|
Pancreatic carcinoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
Lastly, we found that TRIF was required for Ccl2 upregulation in the hypothalamus and induction of the catabolic genes, Mafbx, Murf1, and Foxo1 in gastrocnemius during pancreatic cancer.
|
29852290 |
2018 |
|
Sepsis
|
0.020 |
Biomarker
|
disease |
BEFREE |
These protective effects were mediated through MPLA stimulation of a Toll/IL-1 receptor domain-containing adaptor-inducing IFN-β-(TRIF)-dependent phosphatidylinositol 3-kinase-Akt pathway that prevents sepsis- and LPS-induced ERK activation.
|
29741098 |
2018 |
|
Malignant neoplasm of pancreas
|
0.020 |
Biomarker
|
disease |
BEFREE |
Lastly, we found that TRIF was required for Ccl2 upregulation in the hypothalamus and induction of the catabolic genes, Mafbx, Murf1, and Foxo1 in gastrocnemius during pancreatic cancer.
|
29852290 |
2018 |
|
Respiratory syncytial virus (RSV) infection in conditions classified elsewhere and of unspecified site
|
0.020 |
Biomarker
|
disease |
BEFREE |
We found that the airway inflammatory cells and cytokines present in BALF and TRIF in lung tissue play a role in inducing AHR and airway inflammation upon RSV and bacteria coinfection, which might occur through the TRIF-MMP-9-neutrophil-MMP-9 signalling pathway.
|
28695368 |
2017 |
|
Respiratory syncytial virus (RSV) infection in conditions classified elsewhere and of unspecified site
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
Resveratrol decreased TRIF expression and prevented the RSV-mediated reduction of SARM expression.
|
24478430 |
2014 |
|
Pancreatitis
|
0.020 |
Biomarker
|
disease |
BEFREE |
Our data implicate a primary role for DCs in pancreatic carcinogenesis and illustrate divergent pathways in which blockade of TLR4 signaling via TRIF is protective against pancreatic cancer and, conversely, MyD88 inhibition exacerbates pancreatic inflammation and neoplastic transformation by augmenting the DC-Th2 axis.
|
22908323 |
2012 |
|
Septicemia
|
0.020 |
Biomarker
|
disease |
BEFREE |
Collectively, the results from the current study demonstrate CD16 as a key regulator of the TRIF-dependent TLR4 pathway in human monocytes and their CD16-expressing subset, with implications in sepsis.
|
22427642 |
2012 |
|
Pancreatic carcinoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
Our data implicate a primary role for DCs in pancreatic carcinogenesis and illustrate divergent pathways in which blockade of TLR4 signaling via TRIF is protective against pancreatic cancer and, conversely, MyD88 inhibition exacerbates pancreatic inflammation and neoplastic transformation by augmenting the DC-Th2 axis.
|
22908323 |
2012 |
|
Sepsis
|
0.020 |
Biomarker
|
disease |
BEFREE |
Collectively, the results from the current study demonstrate CD16 as a key regulator of the TRIF-dependent TLR4 pathway in human monocytes and their CD16-expressing subset, with implications in sepsis.
|
22427642 |
2012 |
|
Malignant neoplasm of pancreas
|
0.020 |
Biomarker
|
disease |
BEFREE |
Our data implicate a primary role for DCs in pancreatic carcinogenesis and illustrate divergent pathways in which blockade of TLR4 signaling via TRIF is protective against pancreatic cancer and, conversely, MyD88 inhibition exacerbates pancreatic inflammation and neoplastic transformation by augmenting the DC-Th2 axis.
|
22908323 |
2012 |
|
Acute pancreatitis
|
0.010 |
Biomarker
|
disease |
BEFREE |
TLR3 and its downstream adaptor TICAM1 are important mediators of acinar cell damage in acute pancreatitis.
|
30583980 |
2019 |
|
Hypertensive disease
|
0.010 |
Biomarker
|
group |
BEFREE |
<b>NEW & NOTEWORTHY</b> Angiotensin II (ANG II)-induced hypertension is dependent on the endosomal Toll-like receptor 3 (TLR3)-Toll-interleukin receptor domain-containing adaptor protein-inducing interferon-β (TRIF) pathway of the innate immune system but not on cell membrane localized TLR4.
|
30793936 |
2019 |
|
Van der Woude syndrome
|
0.010 |
Biomarker
|
disease |
BEFREE |
PLAG induced TLR4-mediated TRIF-related adaptor molecules/Toll-interleukin receptor (TIR) domain-containing adaptor protein including interferon (IFN)-β/IRF3 endosomal signaling, leading to rapid association of TRAM/TRIF and TLR4 and earlier IRF3 phosphorylation in PLAG/LPS-treated vs. LPS-treated cells.
|
31620122 |
2019 |
|
Breast Carcinoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
We found a significant unique gene expression signature, such as the Toll-like receptor (TLR) 3- and TLR4-induced Toll/interleukin-1 receptor domain-containing adapter molecule 1 (TICAM1)-specific signaling pathway in the breast cancer patients as compared to that of healthy volunteers.
|
30317464 |
2019 |
|
Amyloidosis
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
For this purpose, the BV-2 cell line was cultured in a 24-well plate, treated with Pam3Cys (1 μg/ml), and then incubated with oligomeric Aβ for 24 h. The expression of TRIF, IRF3, and INFβ was measured by western blot technique.
|
30222725 |
2018 |