INT132278

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.39
First Reported 2005
Last Reported 2010
Negated 2
Speculated 1
Reported most in Body
Documents 32
Total Number 33
Disease Relevance 18.69
Pain Relevance 8.17

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

Golgi apparatus (CTLA4) plasma membrane (CTLA4)
Anatomy Link Frequency
T-cell 10
monocytes 2
dendritic cells 1
regulatory T-cells 1
precursor cells 1
CTLA4 (Homo sapiens)
Pain Link Frequency Relevance Heat
Migraine 7 100.00 Very High Very High Very High
tolerance 76 99.24 Very High Very High Very High
spinal inflammation 41 99.22 Very High Very High Very High
Inflammation 285 99.10 Very High Very High Very High
abatacept 412 99.04 Very High Very High Very High
rheumatoid arthritis 174 98.04 Very High Very High Very High
Arthritis 274 96.48 Very High Very High Very High
Chronic pancreatitis 3 96.28 Very High Very High Very High
psoriasis 320 96.12 Very High Very High Very High
Etanercept 97 94.56 High High
Disease Link Frequency Relevance Heat
Autoimmune Disease 138 100.00 Very High Very High Very High
Diabetes Mellitus 40 100.00 Very High Very High Very High
Headache 13 100.00 Very High Very High Very High
Migraine Without Aura 4 100.00 Very High Very High Very High
Migraine With Aura 4 100.00 Very High Very High Very High
Pancreatitis 15 99.32 Very High Very High Very High
Apoptosis 113 99.24 Very High Very High Very High
Low Back Pain 42 99.22 Very High Very High Very High
INFLAMMATION 299 99.10 Very High Very High Very High
Biliary Liver Cirrhosis 740 99.04 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
To address the poor outcomes in transplantation studies, further development of CTLA4-Ig concentrated on improving its binding to CD86 in particular (owing to its importance in initiation of the immune reaction in primates), in order to confer the more potent immunosuppressive action needed.
CTLA4-Ig Binding (binding) of in CD86
1) Confidence 0.39 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2582812 Disease Relevance 1.04 Pain Relevance 0.49
B7/CTLA-4 interactions and regulatory T-cells
CTLA-4 Binding (interactions) of in regulatory T-cells
2) Confidence 0.36 Published 2007 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2721321 Disease Relevance 0.06 Pain Relevance 0.18
This review is focused on working mechanism of CTLA-4 from its recognition (bench) to its usage as a potential therapeutic agent (bedside) for several inflammatory diseases.
CTLA-4 Binding (recognition) of associated with inflammation and disease
3) Confidence 0.35 Published 2009 Journal Recent patents on inflammation & allergy drug discovery Section Abstract Doc Link 19519585 Disease Relevance 0.71 Pain Relevance 0.47
These data suggest that CTLA-4 is an anti-osteoclastogenic molecule that directly binds osteoclast precursor cells and inhibits their differentiation.
CTLA-4 Binding (binds) of in precursor cells
4) Confidence 0.35 Published 2008 Journal Ann. Rheum. Dis. Section Abstract Doc Link 18203760 Disease Relevance 0.37 Pain Relevance 0.23
CTLA-4 binds to the surface of antigen-presenting cells, such as dendritic cells and monocytes through CD80/86.
CTLA-4 Binding (binds) of in dendritic cells
5) Confidence 0.35 Published 2008 Journal Ann. Rheum. Dis. Section Abstract Doc Link 18203760 Disease Relevance 0.19 Pain Relevance 0.03
Herein, we investigated whether the binding of CTLA-4 affects the differentiation of monocytes into osteoclasts in vitro and vivo.
CTLA-4 Spec (whether) Binding (binding) of in monocytes
6) Confidence 0.35 Published 2008 Journal Ann. Rheum. Dis. Section Abstract Doc Link 18203760 Disease Relevance 0.31 Pain Relevance 0.07
In conclusion, the lack of association between SNPs in the genetic master switches of autoimmunity, PTPN22 and CTLA-4, suggests that regardless of the strong linkage with HLA-B*27, AAU should be regarded as an autoinflammatory rather than an autoimmune condition.



CTLA-4 Binding (association) of associated with autoimmune disease and uveitis
7) Confidence 0.34 Published 2009 Journal Molecular Vision Section Body Doc Link PMC2632733 Disease Relevance 1.07 Pain Relevance 0.05
This functional association between PDCD1 and CTLA4 explains the relationship between PDCD1 and GD, and indicates that the CoPub Discovery predicted association between PDCD1 and GD was correctly identified based on biological knowledge.


CTLA4 Binding (association) of associated with disease
8) Confidence 0.34 Published 2010 Journal PLoS Computational Biology Section Body Doc Link PMC2944780 Disease Relevance 1.20 Pain Relevance 0.27
T-cell regulatory gene CTLA-4 polymorphism/haplotype association with autoimmune pancreatitis.
CTLA-4 Binding (association) of in T-cell associated with pancreatitis
9) Confidence 0.34 Published 2007 Journal Clin. Chem. Section Title Doc Link 17712006 Disease Relevance 0.57 Pain Relevance 0.10
There was no significant association between PTPN22 620W, CTLA-4 ?
CTLA-4 Neg (no) Binding (association) of
10) Confidence 0.33 Published 2009 Journal Molecular Vision Section Abstract Doc Link PMC2632733 Disease Relevance 0.85 Pain Relevance 0.08
Indeed, direct contact between suppressor and effector cells is required in vitro, through the binding of CTLA-4 on T-reg and B7-1/B7-2 on effector cells.
CTLA-4 Binding (binding) of
11) Confidence 0.32 Published 2007 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2721321 Disease Relevance 0 Pain Relevance 0.04
Because CTLA4 has a higher affinity than CD28 for the CD80/86 ligand, it binds to most of the available molecules, effectively shutting down further T cell proliferation.
CTLA4 Binding (binds) of in T cell
12) Confidence 0.30 Published 2010 Journal Drug Design, Development and Therapy Section Body Doc Link PMC2998809 Disease Relevance 0.07 Pain Relevance 0.07
Thus, in abatacept, a series of directed cysteine to serine mutations were introduced in the hinge region to reduce this Fc- mediated binding.21 Although abatacept proved to be highly efficacious for autoimmune T cell-mediated autoimmune disorders, such as rheumatoid arthritis and psoriasis, it was found to be an inadequate maintenance immunosuppressive agent in nonhuman primate models of transplantation.22–24 Studies into potential reasons for this disconnect found that although CTLA4 binds with a much higher avidity to CD80 and CD86 than does CD28, CTLA4-Ig was significantly less potent at inhibiting CD86-dependent as opposed to CD80-dependent costimulation.25
CTLA4 Binding (binds) of in hinge associated with psoriasis, autoimmune disease, rheumatoid arthritis and abatacept
13) Confidence 0.30 Published 2010 Journal Drug Design, Development and Therapy Section Body Doc Link PMC2998809 Disease Relevance 0.29 Pain Relevance 0.39
The most important ligand is CTLA-4, a well-defined down-regulator of T-cell activation, which has a much higher binding affinity for CD80/CD86 than CD28.
CTLA-4 Binding (binding) of in T-cell
14) Confidence 0.30 Published 2008 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2727897 Disease Relevance 0.35 Pain Relevance 0.61
We investigated possible genetic associations of CTLA4 in a Chinese population with AIP.
CTLA4 Binding (associations) of associated with pancreatitis
15) Confidence 0.30 Published 2007 Journal Clin. Chem. Section Abstract Doc Link 17712006 Disease Relevance 0.61 Pain Relevance 0.09
METHODS: We performed genotyping for CTLA4 (49 A/G, -318 C/T, and CT60 A/G) and tumor necrosis factor (TNF)-alpha promoter (-857 C/T, -863 C/A, and -1031 C/T) by use of PCR sequence-specific primers and direct sequencing, respectively, in 46 patients with AIP, 78 patients with chronic calcifying pancreatitis (CCP), and 200 healthy individuals.
CTLA4 Binding (genotyping) of
16) Confidence 0.30 Published 2007 Journal Clin. Chem. Section Body Doc Link 17712006 Disease Relevance 0.10 Pain Relevance 0
The observations that CTLA-4 +49A>G genotypes are associated with circulatory CRP levels and significantly less AS subjects carrying CTLA-4 higher-secretor -318 T allele suggest the level and regulation of inflammation in AS subjects may be pre-determined by and associated with CTLA-4 genotypes.
CTLA-4 Binding (associated) of associated with spinal inflammation and inflammation
17) Confidence 0.30 Published 2010 Journal Tissue Antigens Section Abstract Doc Link 20030788 Disease Relevance 0.85 Pain Relevance 0.82
These results would indicate no association between MA and MO migraine and CTLA-4 polymorphism, excluding any possible role of the CTLA-4 gene as a genetic factor determining susceptibility to migraine.
CTLA-4 Neg (no) Binding (association) of associated with migraine with aura, migraine and migraine without aura
18) Confidence 0.29 Published 2005 Journal J Headache Pain Section Abstract Doc Link 16362660 Disease Relevance 1.20 Pain Relevance 0.63
Key messages

• Lack of success of T-cell-directed therapies has stimulated research into targeting T-cell co-stimulation. • CTLA4-Ig competitively inhibits T-cell activation through its greater binding affinity to the B7 molecules. • Abatacept is a soluble fusion protein that comprises the extracellular domain of human CTLA4 linked to the modified Fc portion of human IgG1. • Clinical trials have demonstrated abatacept to be efficacious in patients with RA who have failed previous DMARDs with radiographic benefit shown in MTX refractory study population. • Trials have also shown abatacept to be an effective option in patients who are refractory to TNF-?

CTLA4-Ig Binding (affinity) of in T-cell associated with rheumatoid arthritis and abatacept
19) Confidence 0.29 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2582812 Disease Relevance 0.27 Pain Relevance 0.64
These two-way B7/CTLA-4 interactions may be involved in the inhibition of T-cell responses.
CTLA-4 Binding (interactions) of in T-cell
20) Confidence 0.28 Published 2007 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2721321 Disease Relevance 0.10 Pain Relevance 0

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox