INT146808

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Context Info
Confidence 0.69
First Reported 2005
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 25
Total Number 25
Disease Relevance 11.98
Pain Relevance 5.71

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 (CCL18) extracellular space (CCL18) extracellular region (CCL18)
cell-cell signaling (CCL18)
Anatomy Link Frequency
Endothelial cells 3
blood 2
T-cell 2
macrophage 1
sputum 1
CCL18 (Homo sapiens)
Pain Link Frequency Relevance Heat
rheumatoid arthritis 908 100.00 Very High Very High Very High
Inflammation 292 100.00 Very High Very High Very High
chemokine 692 99.54 Very High Very High Very High
fibrosis 7 98.48 Very High Very High Very High
Arthritis 24 97.36 Very High Very High Very High
cytokine 117 95.76 Very High Very High Very High
aspirin 10 84.00 Quite High
cINOD 15 65.92 Quite High
antagonist 3 58.44 Quite High
Angina 26 50.00 Quite Low
Disease Link Frequency Relevance Heat
Rheumatoid Arthritis 909 100.00 Very High Very High Very High
INFLAMMATION 344 100.00 Very High Very High Very High
Disease 179 99.68 Very High Very High Very High
Sarcoidosis 41 99.10 Very High Very High Very High
Pulmonary Fibrosis 2 98.48 Very High Very High Very High
Asthma 34 98.44 Very High Very High Very High
Arthritis 27 97.72 Very High Very High Very High
Polyps 26 97.40 Very High Very High Very High
Gauchers Disease 68 96.76 Very High Very High Very High
Rhinitis 124 94.92 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Levels of CC chemokine ligand (CCL)-5 (also known as RANTES [regulated on activation, normally T-cell expressed, and secreted]; 32.7 versus 23.1 ng/mL, P=0.018) and CCL18 (also known as PARC [pulmonary and activation-regulated chemokine]; 104.4 versus 53.7 ng/mL, P=0.011) were significantly elevated in patients with refractory ischemic symptoms versus stabilized patients.
Positive_regulation (elevated) of CCL18 in T-cell
1) Confidence 0.69 Published 2007 Journal Circulation Section Body Doc Link 17909104 Disease Relevance 0.33 Pain Relevance 0
The data therefore indicate that cell–cell contact is crucial for the induction of CCL18.
Positive_regulation (induction) of CCL18
2) Confidence 0.67 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212580 Disease Relevance 0.16 Pain Relevance 0.08
However, CCL18 could be induced by stimulation of SF PMN with IL-10; indeed, IL-10 in combination with vitamin D3 even enhanced CCL18 release.
Positive_regulation (induced) of CCL18
3) Confidence 0.67 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212580 Disease Relevance 0.43 Pain Relevance 0.42
The contribution of PMN to the accumulation of CCL18 in SF is difficult to judge because the cells have a low production rate for cellular mediators.
Positive_regulation (accumulation) of CCL18
4) Confidence 0.67 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212580 Disease Relevance 0.52 Pain Relevance 0.31
Endothelial cells induce CCL18 protein in PMN
Positive_regulation (induce) of CCL18 protein in Endothelial cells
5) Confidence 0.59 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212580 Disease Relevance 0.21 Pain Relevance 0.11
These findings suggest that the high CCL18 levels in SF from RA patients [19] may be induced synergistically, as previously shown for monocytes cultured with IL-10 and SF from patients with RA [35].
Positive_regulation (induced) of CCL18 in monocytes associated with rheumatoid arthritis
6) Confidence 0.49 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212580 Disease Relevance 0.46 Pain Relevance 0.23
Whether a similar ICAM-1-related mechanism accounts for the endothelial cell-mediated induction of CCL18 in PMN is unknown.
Positive_regulation (induction) of CCL18 in endothelial cell
7) Confidence 0.49 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212580 Disease Relevance 0.08 Pain Relevance 0.07
Of these chemokines, the following showed upregulation: CCL18 (4.5 ± 0.4-fold increase), CXCL9 (3.6 ± 0.1-fold increase), CXCL5 (3.5 ± 0.3-fold increase), and CXCL8 (3.3 ± 0.2-fold increase).
Positive_regulation (upregulation) of CCL18 associated with chemokine
8) Confidence 0.48 Published 2005 Journal Arthritis Res Ther Section Body Doc Link PMC1065316 Disease Relevance 1.28 Pain Relevance 1.06
Finally, elevated CCL5 and CCL18 levels predicted future cardiovascular adverse events, whereas C-reactive protein and sCD40L levels did not.
Positive_regulation (elevated) of CCL18
9) Confidence 0.46 Published 2007 Journal Circulation Section Body Doc Link 17909104 Disease Relevance 0 Pain Relevance 0
Levels of CC chemokine ligand (CCL)-5 (also known as RANTES [regulated on activation, normally T-cell expressed, and secreted]; 32.7 versus 23.1 ng/mL, P=0.018) and CCL18 (also known as PARC [pulmonary and activation-regulated chemokine]; 104.4 versus 53.7 ng/mL, P=0.011) were significantly elevated in patients with refractory ischemic symptoms versus stabilized patients.
Positive_regulation (elevated) of PARC in T-cell
10) Confidence 0.46 Published 2007 Journal Circulation Section Body Doc Link 17909104 Disease Relevance 0.33 Pain Relevance 0
In RA, expression of mRNA encoding CCL18 was observed in synovial tissue and it coincided with CCL18 accumulation in SF [19,20].
Positive_regulation (accumulation) of CCL18 associated with rheumatoid arthritis
11) Confidence 0.45 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212580 Disease Relevance 0.34 Pain Relevance 0.55
induces CCL18 mRNA in the absence of CCL18 protein in blood PMN
Positive_regulation (induces) of CCL18 mRNA in blood
12) Confidence 0.45 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212580 Disease Relevance 0.32 Pain Relevance 0.21
Similar levels of CCL18 were released into supernatant of RA blood or SF PMN co-cultured with endothelial cells (data not shown).
Positive_regulation (levels) of CCL18 in endothelial cells associated with rheumatoid arthritis
13) Confidence 0.45 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212580 Disease Relevance 0.17 Pain Relevance 0.08
SF PMN from patients with RA exhibit a characteristic chemokine expression pattern resembling the upregulation of CCL3, CCL18, CXCL8 and CXCL10 mRNAs and the downregulation of CCL21 mRNA.
Positive_regulation (upregulation) of CCL18 associated with chemokine and rheumatoid arthritis
14) Confidence 0.45 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212580 Disease Relevance 0.83 Pain Relevance 0.47
Moreover, because PMN are recruited into SF, a characteristic chemokine expression profile is induced with highly upregulated mRNAs for CCL3, CCL18, CXCL8 and CXCL10 and downregulation of CCL21 mRNA.


Positive_regulation (upregulated) of CCL18 associated with chemokine
15) Confidence 0.45 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212580 Disease Relevance 0.53 Pain Relevance 0.44
As IL-10 and vitamin D3 are known to have anti-inflammatory properties [41,42], the release of CCL18 induced by these mediators might contribute to a suppression of joint inflammation.
Positive_regulation (induced) of CCL18 in joint associated with inflammation and arthritis
16) Confidence 0.45 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212580 Disease Relevance 0.58 Pain Relevance 0.29
Notably, no significant levels of CCL18 mRNA were detectable in blood PMN form RA patients (n = 9; Figure 2b), suggesting that CCL18 gene expression in SF PMN occurs as a result of the recruitment of PMN into the inflammatory milieu of the joint.


Neg (no) Positive_regulation (levels) of CCL18 mRNA in blood associated with inflammation and rheumatoid arthritis
17) Confidence 0.45 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212580 Disease Relevance 0.54 Pain Relevance 0.46
CCL18 values were normalized with HPRT values and are presented as relative gene expression ratios with the 2-??
Positive_regulation (presented) of CCL18
18) Confidence 0.42 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212580 Disease Relevance 0 Pain Relevance 0
Temporal monitoring by ELISA of CCL5, CCL18, and soluble CD40 ligand (sCD40) levels revealed a drop in CCL5 and sCD40L levels in all UAP patients from day 2 onward (CCL5 12.1 ng/mL, P<0.001; sCD40L 1.35 ng/mL, P<0.05), whereas elevated CCL18 levels were sustained for at least 2 days, then were decreased at 180 days after inclusion (34.5 ng/mL, P<0.001).
Positive_regulation (elevated) of CCL18
19) Confidence 0.40 Published 2007 Journal Circulation Section Body Doc Link 17909104 Disease Relevance 0.26 Pain Relevance 0
CCL18 has been reported to be an indicator of pulmonary fibrosis since BAL cells of sarcoidosis patients with X-ray stage IV produce higher levels of CCL18 compared to a lower X-ray stage [29].
Positive_regulation (levels) of CCL18 associated with fibrosis, sarcoidosis and pulmonary fibrosis
20) Confidence 0.40 Published 2010 Journal Respir Res Section Body Doc Link PMC2939603 Disease Relevance 0.42 Pain Relevance 0.16

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