INT175329

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Context Info
Confidence 0.18
First Reported 2003
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 14
Total Number 17
Disease Relevance 10.06
Pain Relevance 2.81

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

cell adhesion (ICAM1, ITGAL) plasma membrane (ICAM1, ITGAL) signal transduction (ITGAL)
extracellular space (ICAM1)
Anatomy Link Frequency
T cells 7
myometrium 2
endothelial cells 2
NK cell 2
cervix 2
ICAM1 (Homo sapiens)
ITGAL (Homo sapiens)
Pain Link Frequency Relevance Heat
psoriasis 383 96.92 Very High Very High Very High
Multiple sclerosis 20 95.40 Very High Very High Very High
cytokine 203 94.00 High High
Inflammation 164 93.60 High High
endometriosis 198 84.60 Quite High
Restless leg syndrome 2 77.76 Quite High
Inflammatory response 7 73.60 Quite High
backache 1 73.04 Quite High
abatacept 9 68.72 Quite High
Pain 15 66.52 Quite High
Disease Link Frequency Relevance Heat
Endometriosis 252 100.00 Very High Very High Very High
Adhesions 80 100.00 Very High Very High Very High
Infection 106 99.50 Very High Very High Very High
Acquired Immune Deficiency Syndrome Or Hiv Infection 286 99.26 Very High Very High Very High
Leukocytosis 4 98.58 Very High Very High Very High
Psoriasis 445 96.92 Very High Very High Very High
Demyelinating Disease 31 95.40 Very High Very High Very High
INFLAMMATION 166 93.60 High High
Disease Progression 11 93.36 High High
Encephalitis 1 89.96 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
This drug binds to CD11a on T cells blocking the interaction between LFA-1 and intercellular adhesion molecule 1 (ICAM-1), its partner molecule for adhesion.
ICAM-1 Binding (interaction) of LFA-1 in T cells associated with adhesions
1) Confidence 0.18 Published 2007 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2721342 Disease Relevance 0.32 Pain Relevance 0.03
This drug binds to CD11a on T cells blocking the interaction between LFA-1 and intercellular adhesion molecule 1 (ICAM-1), its partner molecule for adhesion.
intercellular adhesion molecule 1 Binding (interaction) of LFA-1 in T cells associated with adhesions
2) Confidence 0.18 Published 2007 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2721342 Disease Relevance 0.32 Pain Relevance 0.03
Efalizumab is a humanized monoclonal IgG antibody that binds to the alpha-subunit (CD11) of LFA-1 and prevents LFA-1 binding to ICAM-1.
ICAM-1 Binding (binding) of LFA-1
3) Confidence 0.05 Published 2005 Journal J Immune Based Ther Vaccines Section Body Doc Link PMC1208938 Disease Relevance 1.25 Pain Relevance 0.38
Neutrophil and monocyte adhesion to myometrial and cervical endothelium will be promoted during parturition by the increased CD11a and CD11b expression which we demonstrated: CD11a and b mediate binding to ICAM-1, which we previously showed was up-regulated in endothelium of human cervix and myometrium during labour (Ledingham et al., 2001).
ICAM-1 Binding (binding) of CD11a in cervix associated with adhesions
4) Confidence 0.04 Published 2009 Journal Molecular Human Reproduction Section Body Doc Link PMC2762373 Disease Relevance 0.10 Pain Relevance 0.03
Neutrophil and monocyte adhesion to myometrial and cervical endothelium will be promoted during parturition by the increased CD11a and CD11b expression which we demonstrated: CD11a and b mediate binding to ICAM-1, which we previously showed was up-regulated in endothelium of human cervix and myometrium during labour (Ledingham et al., 2001).
ICAM-1 Binding (binding) of CD11a in cervix associated with adhesions
5) Confidence 0.04 Published 2009 Journal Molecular Human Reproduction Section Body Doc Link PMC2762373 Disease Relevance 0.10 Pain Relevance 0.03
Therefore, the pathogenesis of HIV-1 infection can be modulated by the ICAM-1/LFA-1 interaction through modulatory effects on cell to-cell transmission of HIV-1, virus replication, virus-mediated syncytium formation, depletion of CD4 T cells, and destruction of the architecture of secondary lymphoid organs [57-62].
ICAM-1 Binding (interaction) of LFA-1 in T cells associated with acquired immune deficiency syndrome or hiv infection and infection
6) Confidence 0.03 Published 2009 Journal Trials Section Body Doc Link PMC2705367 Disease Relevance 0.87 Pain Relevance 0
The third mechanism is unrelated to inhibition of HMG-CoA reductase, and consist in blocking the interaction between LFA-1 and ICAM-1 adhesion molecules [30], which is crucial to stabilize antigen presenting cell/T-cell contact during antigen presentation and to regulate the traffic of leukocytes during homeostatic and inflammatory conditions [31,32].
ICAM-1 Binding (interaction) of LFA-1 in T-cell associated with inflammation and adhesions
7) Confidence 0.03 Published 2009 Journal Trials Section Body Doc Link PMC2705367 Disease Relevance 0.44 Pain Relevance 0.11
Therefore, the pathogenesis of HIV-1 infection can be modulated by the ICAM-1/LFA-1 interaction through modulatory effects on cell to-cell transmission of HIV-1, virus replication, virus-mediated syncytium formation, depletion of CD4 T cells, and destruction of the architecture of secondary lymphoid organs [57-62].
ICAM-1 Binding (interaction) of LFA-1 in T cells associated with acquired immune deficiency syndrome or hiv infection and infection
8) Confidence 0.03 Published 2009 Journal Trials Section Body Doc Link PMC2705367 Disease Relevance 0.87 Pain Relevance 0
Neutrophil and monocyte adhesion to myometrial and cervical endothelium will be promoted during parturition by the increased CD11a and CD11b expression which we demonstrated: CD11a and b mediate binding to ICAM-1, which we previously showed was up-regulated in endothelium of human cervix and myometrium during labour (Ledingham et al., 2001).
ICAM-1 Binding (binding) of CD11a in myometrium associated with adhesions
9) Confidence 0.02 Published 2009 Journal Molecular Human Reproduction Section Body Doc Link PMC2762373 Disease Relevance 0.10 Pain Relevance 0.03
Neutrophil and monocyte adhesion to myometrial and cervical endothelium will be promoted during parturition by the increased CD11a and CD11b expression which we demonstrated: CD11a and b mediate binding to ICAM-1, which we previously showed was up-regulated in endothelium of human cervix and myometrium during labour (Ledingham et al., 2001).
ICAM-1 Binding (binding) of CD11a in myometrium associated with adhesions
10) Confidence 0.02 Published 2009 Journal Molecular Human Reproduction Section Body Doc Link PMC2762373 Disease Relevance 0.10 Pain Relevance 0.03
In a longterm clinical study, 50% of 228 patients with chronic plaque psoriasis achieved PASI 75 after 15 months of continuous efalizumab treatment, suggesting sustained efficacy with efalizumab.[24] Efalizumab was approved for treatment of psoriasis by FDA in 2003.[25] Administration of efalizumab induces a peripheral leukocytosis (predominantly of CD8+ memory cells), which is due to blockade of the LFA-1/ICAM-1 interaction between T cells and endothelial cells.
ICAM-1 Binding (interaction) of LFA-1 in endothelial cells associated with psoriasis and leukocytosis
11) Confidence 0.01 Published 2008 Journal Indian Journal of Pharmacology Section Body Doc Link PMC2792605 Disease Relevance 0.47 Pain Relevance 0.27
In a longterm clinical study, 50% of 228 patients with chronic plaque psoriasis achieved PASI 75 after 15 months of continuous efalizumab treatment, suggesting sustained efficacy with efalizumab.[24] Efalizumab was approved for treatment of psoriasis by FDA in 2003.[25] Administration of efalizumab induces a peripheral leukocytosis (predominantly of CD8+ memory cells), which is due to blockade of the LFA-1/ICAM-1 interaction between T cells and endothelial cells.
ICAM-1 Binding (interaction) of LFA-1 in endothelial cells associated with psoriasis and leukocytosis
12) Confidence 0.01 Published 2008 Journal Indian Journal of Pharmacology Section Body Doc Link PMC2792605 Disease Relevance 0.47 Pain Relevance 0.27
Lovastatin treatment also attenuated the transmigration of mononuclear cells by downregulating the expression of leukocyte function antigen-1 (LFA-1), a ligand for intercellular adhesion molecule (ICAM), in endothelial-leukocyte interaction [88] and mononuclear cell infiltration into the CNS has been implicated in MS [89].
ICAM Binding (ligand) of LFA-1 in leukocyte associated with multiple sclerosis and adhesions
13) Confidence 0.01 Published 2005 Journal J Negat Results Biomed Section Body Doc Link PMC1079931 Disease Relevance 1.63 Pain Relevance 0.61
Soluble forms of ICAM-1 (s-ICAM-1) secreted by PF endometrial cells/endometriotic lesions can also bind to LFA-1 presenting lymphocytes and could prevent the recognition of endometrial cells by these lymphocytes and prevent subsequent NK cell-mediated cytotoxicity [57,58].
s-ICAM-1 Binding (bind) of LFA-1 in NK cell associated with endometriosis
14) Confidence 0.01 Published 2003 Journal Reprod Biol Endocrinol Section Body Doc Link PMC305339 Disease Relevance 1.00 Pain Relevance 0.21
Soluble forms of ICAM-1 (s-ICAM-1) secreted by PF endometrial cells/endometriotic lesions can also bind to LFA-1 presenting lymphocytes and could prevent the recognition of endometrial cells by these lymphocytes and prevent subsequent NK cell-mediated cytotoxicity [57,58].
ICAM-1 Binding (bind) of LFA-1 in NK cell associated with endometriosis
15) Confidence 0.01 Published 2003 Journal Reprod Biol Endocrinol Section Body Doc Link PMC305339 Disease Relevance 1.00 Pain Relevance 0.21
In a longterm clinical study, 50% of 228 patients with chronic plaque psoriasis achieved PASI 75 after 15 months of continuous efalizumab treatment, suggesting sustained efficacy with efalizumab.[24] Efalizumab was approved for treatment of psoriasis by FDA in 2003.[25] Administration of efalizumab induces a peripheral leukocytosis (predominantly of CD8+ memory cells), which is due to blockade of the LFA-1/ICAM-1 interaction between T cells and endothelial cells.
ICAM-1 Binding (interaction) of LFA-1 in T cells associated with psoriasis and leukocytosis
16) Confidence 0.00 Published 2008 Journal Indian Journal of Pharmacology Section Body Doc Link PMC2792605 Disease Relevance 0.47 Pain Relevance 0.27
In a longterm clinical study, 50% of 228 patients with chronic plaque psoriasis achieved PASI 75 after 15 months of continuous efalizumab treatment, suggesting sustained efficacy with efalizumab.[24] Efalizumab was approved for treatment of psoriasis by FDA in 2003.[25] Administration of efalizumab induces a peripheral leukocytosis (predominantly of CD8+ memory cells), which is due to blockade of the LFA-1/ICAM-1 interaction between T cells and endothelial cells.
ICAM-1 Binding (interaction) of LFA-1 in T cells associated with psoriasis and leukocytosis
17) Confidence 0.00 Published 2008 Journal Indian Journal of Pharmacology Section Body Doc Link PMC2792605 Disease Relevance 0.47 Pain Relevance 0.27

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