INT142593

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Context Info
Confidence 0.70
First Reported 2007
Last Reported 2010
Negated 2
Speculated 1
Reported most in Body
Documents 85
Total Number 87
Disease Relevance 75.90
Pain Relevance 13.62

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

signal transduction (Tlr2) plasma membrane (Tlr2) intracellular (Tlr2)
cytoplasm (Tlr2)
Anatomy Link Frequency
microglia 6
kidney 3
neutrophil 3
TECs 3
T cell 3
Tlr2 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 1515 100.00 Very High Very High Very High
agonist 165 99.96 Very High Very High Very High
cytokine 853 99.84 Very High Very High Very High
rheumatoid arthritis 232 99.78 Very High Very High Very High
chemokine 299 99.68 Very High Very High Very High
ischemia 150 99.52 Very High Very High Very High
fibrosis 494 99.44 Very High Very High Very High
alcohol 24 99.32 Very High Very High Very High
tolerance 143 98.44 Very High Very High Very High
antagonist 72 97.36 Very High Very High Very High
Disease Link Frequency Relevance Heat
INFLAMMATION 1707 100.00 Very High Very High Very High
Injury 1450 100.00 Very High Very High Very High
Hydronephrosis 1001 100.00 Very High Very High Very High
Renal Disease 468 100.00 Very High Very High Very High
Ureteral Obstruction 468 100.00 Very High Very High Very High
Infection 457 100.00 Very High Very High Very High
Stress 130 100.00 Very High Very High Very High
Rheumatoid Arthritis 232 99.78 Very High Very High Very High
Premature Birth 51 99.74 Very High Very High Very High
Internal Fibrosis 117 99.68 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Together, these data suggests that the activation of TLR2 on tubular epithelial and interstitial cells by endogenous stress ligands may play a role in renal inflammation, and apoptosis during progressive renal injury.
Positive_regulation (activation) of TLR2 in interstitial cells associated with stress, hydronephrosis, inflammation, injury and apoptosis
1) Confidence 0.70 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2682651 Disease Relevance 1.50 Pain Relevance 0.31
Activation of TLR2 signaling was essential for two key stages in priming immune responses against brain tumor antigen: (1) the migration of peripheral DC into the brain tumor, and (2) the subsequent activation of DC and stimulation of tumor antigen specific T cell clonal expansion.
Positive_regulation (Activation) of TLR2 in T cell associated with cancer and brain tumor
2) Confidence 0.68 Published 2009 Journal PLoS Medicine Section Body Doc Link PMC2621261 Disease Relevance 1.09 Pain Relevance 0.13
Secondly, HSP60 activation of TLR2 mediates the expression and phosphorylation of Stat3 in tumor cells.
Positive_regulation (activation) of TLR2 associated with cancer
3) Confidence 0.64 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2716531 Disease Relevance 0.73 Pain Relevance 0.04
Our studies not only demonstrate that targeting TLR2 generates metastases clearing immunity, but also reveals a signal transduction pathway in the tumor by which HSP60 liberated from B16 cells, causes a persistent activation of TLR2 to maintain the constitutive activity and function of Stat3 in these cells and determine the development of tumor immune tolerance.
Positive_regulation (activation) of TLR2 associated with cancer, tolerance and metastasis
4) Confidence 0.64 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2716531 Disease Relevance 0.91 Pain Relevance 0.05
Fourthly, the TLR2 activation of Stat3 is partially dependent of IL-6 and IL-10.
Positive_regulation (activation) of TLR2
5) Confidence 0.64 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2716531 Disease Relevance 0.60 Pain Relevance 0.03
Importantly, heat shock protein 60 released by tumor cells caused a persistent activation of TLR2 and was critical in the constitutive activation of transcription factor Stat3, leading to the release of immunosuppressive cytokines and chemokines.
Positive_regulation (activation) of TLR2 associated with chemokine, cancer, shock and cytokine
6) Confidence 0.64 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2716531 Disease Relevance 1.23 Pain Relevance 0.13
Our results are supported by the recent report by Huang et al. in which activation of TLR2 by Listeria monocytogenes promotes tumor growth [3].
Positive_regulation (activation) of TLR2 associated with cancer
7) Confidence 0.64 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2716531 Disease Relevance 1.24 Pain Relevance 0.03
Importantly, the endogenous ligands that can activate TLR2 and TLR4 are strongly upregulated in these TECs upon I/R injury [15].
Positive_regulation (activate) of TLR2 in TECs associated with injury
8) Confidence 0.56 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2570789 Disease Relevance 0.63 Pain Relevance 0.09
Activation of TLR2 by LPS significantly enhanced the expression of TLR2 on these cells (Figure S1E).
Positive_regulation (Activation) of TLR2
9) Confidence 0.56 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2716531 Disease Relevance 0.19 Pain Relevance 0.18
Together, these data suggest that progressive renal injury leads to a marked enhancement of TLR2 and several main endogenous stress ligands.


Positive_regulation (enhancement) of TLR2 associated with stress and injury
10) Confidence 0.50 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2682651 Disease Relevance 1.71 Pain Relevance 0.04
To test the hypothesis that HMGB1 secreted from GBM-bearing mice after treatment with Flt3L plus TK (GCV) mediates TLR2 signaling and T cell-dependent brain tumor regression in vivo, we blocked circulating HMGB1 in vivo using glycyrrhizin or specific anti-HMGB1 immunoglobulins.
Positive_regulation (mediates) of TLR2 in T cell associated with glioblastoma and brain tumor
11) Confidence 0.49 Published 2009 Journal PLoS Medicine Section Body Doc Link PMC2621261 Disease Relevance 0.73 Pain Relevance 0.03
2 = 0.49; Figure 7C), suggesting that HMGB1 released from dying tumor cells might be responsible for activating TLR2 on DC in vivo and subsequent T cell-dependent tumor regression.
Positive_regulation (activating) of TLR2 in T cell associated with cancer
12) Confidence 0.49 Published 2009 Journal PLoS Medicine Section Body Doc Link PMC2621261 Disease Relevance 0.75 Pain Relevance 0.04
To investigate whether HMGB1, released from dying GL26 tumor cells (Ad-TK + GCV treated), was responsible for TLR2 activation in vitro, we inhibited HMGB1 binding using glycyrrhizin, a known antagonist of HMGB1 [40,63].
Positive_regulation (activation) of TLR2 associated with cancer and antagonist
13) Confidence 0.49 Published 2009 Journal PLoS Medicine Section Body Doc Link PMC2621261 Disease Relevance 0.95 Pain Relevance 0.05
This strongly suggests that HMGB1 is the main, if not unique, endogenous activator of TLR2 signaling and necessary innate immune activation.
Positive_regulation (activation) of TLR2
14) Confidence 0.49 Published 2009 Journal PLoS Medicine Section Body Doc Link PMC2621261 Disease Relevance 0.73 Pain Relevance 0.03
Here we show that dying glioma cells released HMGB1, as a result of infection and killing with Ad-TK (+GCV); HMGB1 in turn stimulated TLR2-dependent NF?
Positive_regulation (stimulated) of TLR2 associated with infection and glioma
15) Confidence 0.49 Published 2009 Journal PLoS Medicine Section Body Doc Link PMC2621261 Disease Relevance 1.01 Pain Relevance 0.03
In the absence of HBeAg, HBV replication is associated with upregulation of the TLR2 pathway, leading to increased TNF?
Positive_regulation (upregulation) of TLR2 associated with hepatitis b virus infection
16) Confidence 0.48 Published 2010 Journal Gastroenterology Research and Practice Section Body Doc Link PMC2995932 Disease Relevance 1.36 Pain Relevance 0.12
The expression and function of TLR2 during renal fibrosis and chronic inflammation has however not yet been elucidated.
Positive_regulation (function) of TLR2 associated with fibrosis, inflammation and internal fibrosis
17) Confidence 0.47 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2682651 Disease Relevance 1.13 Pain Relevance 0.29
Our results demonstrate that TLR2 and its main stress ligands are markedly upregulated in the kidney after UUO-injury, obstructive hydronephrosis (TLR2) and IgA nephropathy (TLR2) and identify TLR2 as an initiator of renal inflammation (neutrophil influx, cytokine induction) during progressive renal injury.
Positive_regulation (upregulated) of TLR2 in neutrophil associated with hydronephrosis, stress, ureteral obstruction, inflammation, renal disease, injury and cytokine
18) Confidence 0.47 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2682651 Disease Relevance 3.02 Pain Relevance 0.35
Recently, it was shown that Toll-like receptor 2 (TLR2) is expressed in the kidney and activated by endogenous danger signals.
Positive_regulation (activated) of Toll-like receptor 2 in kidney
19) Confidence 0.47 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2682651 Disease Relevance 1.06 Pain Relevance 0.26
TLR2 protein was markedly upregulated 3, 7 and 14 after UUO-injury in kidneys of TLR2+/+ mice as compared with the contralateral unobstructed kidneys (Fig. 2B).
Positive_regulation (upregulated) of TLR2 protein associated with ureteral obstruction and injury
20) Confidence 0.47 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2682651 Disease Relevance 0.95 Pain Relevance 0.05

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