INT97134

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Context Info
Confidence 0.57
First Reported 2001
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 8
Total Number 10
Disease Relevance 5.09
Pain Relevance 2.11

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

plasma membrane (CD80) intracellular (CD80) cell-cell signaling (CD80)
Anatomy Link Frequency
CD86 2
B-cells 2
T cells 2
dendritic cells 1
cytotoxic T-cell 1
CD80 (Homo sapiens)
Pain Link Frequency Relevance Heat
abatacept 90 99.08 Very High Very High Very High
rheumatoid arthritis 76 96.56 Very High Very High Very High
psoriasis 73 93.72 High High
cytokine 120 84.88 Quite High
Inflammation 80 74.64 Quite High
Arthritis 17 63.20 Quite High
methotrexate 5 19.84 Low Low
Infliximab 15 5.00 Very Low Very Low Very Low
Etanercept 13 5.00 Very Low Very Low Very Low
tolerance 11 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Anaerobic Bacterial Infections 32 99.48 Very High Very High Very High
Cancer 544 98.92 Very High Very High Very High
Adhesions 10 98.48 Very High Very High Very High
Rheumatoid Arthritis 76 96.56 Very High Very High Very High
Apoptosis 25 95.52 Very High Very High Very High
Psoriasis 81 93.72 High High
Renal Cancer 15 93.32 High High
Viremia 2 93.12 High High
Organ Transplantation 1 93.04 High High
Infection 57 91.40 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Abatacept is a recombinant soluble fusion protein that inhibits the CD80/CD86:CD28 costimulatory signal required for T cell activation and has demonstrated efficacy in the treatment of rheumatoid arthritis.
Negative_regulation (inhibits) of CD80 in T cell associated with rheumatoid arthritis and abatacept
1) Confidence 0.57 Published 2007 Journal J Clin Pharmacol Section Abstract Doc Link 17962428 Disease Relevance 0.33 Pain Relevance 0.39
Abatacept attenuates T cell activation as it regulates the activation of T cells by inhibiting the CD80/86:CD28 co-stimulatory pathway that is required for the proper T cell activation.
Negative_regulation (inhibiting) of CD80 in T cells associated with abatacept
2) Confidence 0.41 Published 2009 Journal Basic Clin. Pharmacol. Toxicol. Section Abstract Doc Link 19228144 Disease Relevance 0.59 Pain Relevance 0.75
The inhibition of the CD80/CD86:CD28 co-stimulatory signal may also potentially prevent the T-cell 'help' needed for optimal differentiation of CD80/CD86-expressing B cells into plasma cells, which ultimately secrete antibodies.
Negative_regulation (inhibition) of CD80 in B cells
3) Confidence 0.37 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC1906816 Disease Relevance 0.17 Pain Relevance 0.55
In distinction to drug-free maturing dendritic cells, 2.5 micromol/L sulfasalazine upregulated the levels of CD14 and CD68 and downregulated the levels of CD40, CD80, and CD83 (for all CD markers, p<0.03 for difference between measurements in the absence and the presence of sulfasalazine).
Negative_regulation (downregulated) of CD80 in dendritic cells
4) Confidence 0.33 Published 2001 Journal Croat. Med. J. Section Body Doc Link 11471196 Disease Relevance 0 Pain Relevance 0
This loss was also demonstrated by decreases in CD80-, 86- and 95-expressing B-cells in these three organs.
Negative_regulation (decreases) of CD80 in B-cells
5) Confidence 0.30 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2695011 Disease Relevance 0.57 Pain Relevance 0.05
Inhibition of CD28-mediated co-stimulatory signals is a potent means of immunosuppression that can be achieved by blocking either CD28 or CD80 and CD86.
Negative_regulation (blocking) of CD80 in CD86
6) Confidence 0.18 Published 2005 Journal Arthritis Res Ther Section Body Doc Link PMC2833981 Disease Relevance 0.82 Pain Relevance 0.22
In addition, the LC also acquires a number of cell surface receptor markers such as CD80, CD86, CD40, CD83, and intercellular adhesion molecule (ICAM) 1.
Negative_regulation (number) of CD80 in CD86 associated with adhesions
7) Confidence 0.16 Published 2008 Journal Indian Journal of Pharmacology Section Body Doc Link PMC2792605 Disease Relevance 0.42 Pain Relevance 0.15
It has been demonstrated that B7-H4 can inhibit T-cell proliferation and IL-2 production, and that blockade of B7-H4 in preclinical animal models results in enhanced cytotoxic T-cell responses against an alloantigen [19].
Negative_regulation (blockade) of B7 in cytotoxic T-cell
8) Confidence 0.07 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2840411 Disease Relevance 0.75 Pain Relevance 0
In preclinical studies, blockade of B7-H1 with a specific monoclonal antibody has resulted in enhanced antitumor immune responses [93, 94].
Negative_regulation (blockade) of B7
9) Confidence 0.07 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2840411 Disease Relevance 0.70 Pain Relevance 0
Therefore, blocking of molecules such as B7-H1 and B7-H4 expressed on tumor cells can reduce coinhibitory signals directly at the site of the tumor (Table 3), resulting in enhanced antitumor immune responses.
Negative_regulation (blocking) of B7 associated with cancer
10) Confidence 0.07 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2840411 Disease Relevance 0.73 Pain Relevance 0

General Comments

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