CIDeRplusGeneral Information:
| Id: | 4,119 |
| Diseases: |
Glaucoma
Infantile spasm Multiple sclerosis - [OMIM] |
| Mammalia | |
| review | |
| Reference: | Ross AP et al.(2013) Multiple sclerosis, relapses, and the mechanism of action of adrenocorticotropic hormone Front Neurol 4: 21 [PMID: 23482896] |
Interaction Information:
| Comment | High-dose corticosteroids are the standard of care for treating MS relapses. Corticosteroid treatment shortens the time to recovery from relapses, presumably due at least in part to their anti-inflammatory effects. |
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Formal Description Interaction-ID: 42431 |
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| Comment | PLEX (plasmapheresis / plasma exchange) is generally reserved for treatment of relapses that are severe or refractory to treatment with high-dose corticosteroids or ACTH, as evidence of its clinical efficacy is limited. |
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Formal Description Interaction-ID: 42595 |
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| Comment | For relapses that require treatment, options include high-dose corticosteroids, ACTH gel, and IVIG (intravenous immunoglobulins). |
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Formal Description Interaction-ID: 42596 |
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| Comment | Adrenocorticotropic hormone (ACTH) gel (Acthar Gel), a long-acting formulation of the full sequence ACTH (1-39) that includes other pro-opiomelanocortin (POMC) peptides, is considered an alternative to steroids in treatment of optic neuritis and acute exacerbations of MS. ACTH effects were believed to depend on induction of endogenous corticosteroid production, but ACTH has been shown to be effective in the treatment of infantile spasms (IS), a condition in which corticosteroid treatment has limited effectiveness. |
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Formal Description Interaction-ID: 42597 |
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| Drugbank entries | Show/Hide entries for Corticotropin |
| Comment | Adrenocorticotropic hormone (ACTH) gel (Acthar Gel), a long-acting formulation of the full sequence ACTH (1-39) that includes other pro-opiomelanocortin (POMC) peptides, is considered an alternative to steroids in treatment of optic neuritis and acute exacerbations of MS. ACTH effects were believed to depend on induction of endogenous corticosteroid production, but ACTH has been shown to be effective in the treatment of infantile spasms (IS), a condition in which corticosteroid treatment has limited effectiveness. |
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Formal Description Interaction-ID: 42598 |
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| Drugbank entries | Show/Hide entries for Corticotropin |
| Comment | Adrenocorticotropic hormone (ACTH) gel (Acthar Gel), a long-acting formulation of the full sequence ACTH (1-39) that includes other pro-opiomelanocortin (POMC) peptides, is considered an alternative to steroids in treatment of optic neuritis and acute exacerbations of MS. ACTH effects were believed to depend on induction of endogenous corticosteroid production, but ACTH has been shown to be effective in the treatment of infantile spasms (IS), a condition in which corticosteroid treatment has limited effectiveness. |
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Formal Description Interaction-ID: 42599 |
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| Drugbank entries | Show/Hide entries for Corticotropin |
| Comment | Multiple sclerosis is an immune-mediated disease leading to CNS inflammation, demyelination, and degeneration. |
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Formal Description Interaction-ID: 42600 |
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| Comment | Multiple sclerosis is an immune-mediated disease leading to CNS inflammation, demyelination, and degeneration. |
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Formal Description Interaction-ID: 42601 |
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| Comment | Multiple sclerosis is an immune-mediated disease leading to CNS inflammation, demyelination, and degeneration. |
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Formal Description Interaction-ID: 42602 |
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| Comment | Chronic demyelination, axonal loss, and gliosis (i.e., a proliferation of astrocytes in damaged areas of the CNS, which usually leads to the formation of a glial scar) are associated, although not exclusively, with progressive MS, and are believed to contribute to chronic neurologic deficits. |
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Formal Description Interaction-ID: 42603 |
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| Comment | Chronic demyelination, axonal loss, and gliosis (i.e., a proliferation of astrocytes in damaged areas of the CNS, which usually leads to the formation of a glial scar) are associated, although not exclusively, with progressive MS, and are believed to contribute to chronic neurologic deficits. |
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Formal Description Interaction-ID: 42604 |
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| Comment | Chronic demyelination, axonal loss, and gliosis (i.e., a proliferation of astrocytes in damaged areas of the CNS, which usually leads to the formation of a glial scar) are associated, although not exclusively, with progressive MS, and are believed to contribute to chronic neurologic deficits. |
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Formal Description Interaction-ID: 42605 |
disease increases_activity of process |
| Comment | Myelin, which is formed by oligodendrocytes in the CNS, surrounds and protects axons while functioning to facilitate signal conduction along the axon. Myelin damage leads to conduction slowing or completely blocked conduction, which underlies the clinical presentation of relapses. |
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Formal Description Interaction-ID: 42606 |
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| Comment | Increased blood-brain barrier (BBB) permeability is a hallmark of MS and is a key factor in the inflammatory process leading to demyelination and formation of MS lesions. |
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Formal Description Interaction-ID: 42617 |
disease increases_activity of phenotype increased blood-brain barrier permeability |
| Comment | Increased blood-brain barrier (BBB) permeability is a hallmark of MS and is a key factor in the inflammatory process leading to demyelination and formation of MS lesions. |
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Formal Description Interaction-ID: 42618 |
phenotype increased blood-brain barrier permeability increases_activity of process |
| Comment | Increased blood-brain barrier (BBB) permeability is a hallmark of MS and is a key factor in the inflammatory process leading to demyelination and formation of MS lesions. |
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Formal Description Interaction-ID: 42619 |
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| Comment | Increased BBB (blood-brain barrier) permeability allows infiltration of proinflammatory cells (e.g. T-cells and B-cells) into the CNS. |
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Formal Description Interaction-ID: 42620 |
phenotype increased blood-brain barrier permeability increases_transport of tissue/cell line |
| Comment | Increased BBB (blood-brain barrier) permeability allows infiltration of proinflammatory cells (e.g. T-cells and B-cells) into the CNS. |
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Formal Description Interaction-ID: 42621 |
phenotype increased blood-brain barrier permeability increases_transport of tissue/cell line |
| Comment | Oligodendrocytes are localized in the CNS. |
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Formal Description Interaction-ID: 42632 |
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| Comment | Penetration of immune cells into the CNS is promoted by enhanced expression of adhesion molecules and release of chemokines (e.g. CCL2, CCL5, CXCL1, CXCL2). |
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Formal Description Interaction-ID: 42633 |
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| Comment | Penetration of immune cells into the CNS is promoted by enhanced expression of adhesion molecules and release of chemokines (e.g. CCL2, CCL5, CXCL1, CXCL2). |
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Formal Description Interaction-ID: 42634 |
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| Comment | Penetration of immune cells into the CNS is promoted by enhanced expression of adhesion molecules and release of chemokines (e.g. CCL2, CCL5, CXCL1, CXCL2). |
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Formal Description Interaction-ID: 42635 |
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| Drugbank entries | Show/Hide entries for CCL2 |
| Comment | Penetration of immune cells into the CNS is promoted by enhanced expression of adhesion molecules and release of chemokines (e.g. CCL2, CCL5, CXCL1, CXCL2). |
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Formal Description Interaction-ID: 42636 |
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| Drugbank entries | Show/Hide entries for CCL2 |
| Comment | CCL2 is part of chemokines. |
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Formal Description Interaction-ID: 42637 |
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| Drugbank entries | Show/Hide entries for CCL2 |
| Comment | CCL5 is part of chemokines. |
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Formal Description Interaction-ID: 42638 |
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| Drugbank entries | Show/Hide entries for CCL5 |
| Comment | Penetration of immune cells into the CNS is promoted by enhanced expression of adhesion molecules and release of chemokines (e.g. CCL2, CCL5, CXCL1, CXCL2). |
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Formal Description Interaction-ID: 42639 |
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| Drugbank entries | Show/Hide entries for CCL5 |
| Comment | Penetration of immune cells into the CNS is promoted by enhanced expression of adhesion molecules and release of chemokines (e.g. CCL2, CCL5, CXCL1, CXCL2). |
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Formal Description Interaction-ID: 42640 |
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| Drugbank entries | Show/Hide entries for CCL5 |
| Comment | CXCL1 is part of chemokines. |
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Formal Description Interaction-ID: 42641 |
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| Comment | Penetration of immune cells into the CNS is promoted by enhanced expression of adhesion molecules and release of chemokines (e.g. CCL2, CCL5, CXCL1, CXCL2). |
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Formal Description Interaction-ID: 42642 |
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| Comment | Penetration of immune cells into the CNS is promoted by enhanced expression of adhesion molecules and release of chemokines (e.g. CCL2, CCL5, CXCL1, CXCL2). |
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Formal Description Interaction-ID: 42643 |
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| Comment | CXCL2 is part of chemokines. |
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Formal Description Interaction-ID: 42644 |
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| Comment | Penetration of immune cells into the CNS is promoted by enhanced expression of adhesion molecules and release of chemokines (e.g. CCL2, CCL5, CXCL1, CXCL2). |
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Formal Description Interaction-ID: 42645 |
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| Comment | Penetration of immune cells into the CNS is promoted by enhanced expression of adhesion molecules and release of chemokines (e.g. CCL2, CCL5, CXCL1, CXCL2). |
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Formal Description Interaction-ID: 42646 |
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| Comment | Increased BBB (blood-brain barrier) permeability allows infiltration of proinflammatory cells (e.g. T-cells and B-cells) into the CNS. |
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Formal Description Interaction-ID: 42647 |
phenotype increased blood-brain barrier permeability increases_activity of phenotype |
| Comment | Demyelination involves several types of immune cells (e.g.T-cells, B-cells, and macrophages / monocytes) and inflammatory mediators (e.g.cytokines and chemokines). |
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Formal Description Interaction-ID: 42648 |
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| Comment | Demyelination involves several types of immune cells (e.g.T-cells, B-cells, and macrophages / monocytes) and inflammatory mediators (e.g.cytokines and chemokines). |
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Formal Description Interaction-ID: 42653 |
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| Comment | Demyelination involves several types of immune cells (e.g.T-cells, B-cells, and macrophages / monocytes) and inflammatory mediators (e.g.cytokines and chemokines). |
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Formal Description Interaction-ID: 42654 |
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| Comment | Multiple sclerosis (MS) is an inflammatory demyelinating CNS disease. |
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Formal Description Interaction-ID: 42655 |
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| Comment | Multiple sclerosis (MS) is an inflammatory demyelinating CNS disease. |
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Formal Description Interaction-ID: 42656 |
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| Comment | Oligodendrocytes are damaged by inflammatory processes. Therefore remyelination is often incomplete. |
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Formal Description Interaction-ID: 42657 |
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| Comment | Myelin oligodendrocyte glycoprotein (MOG), a membrane protein, is expressed on oligodendrocytes. |
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Formal Description Interaction-ID: 42658 |
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| Comment | CD4+ T helper cells (i.e.Th1, Th2, and Th17 cells) and CD8+ T cells have been shown to be present in MS lesions and are implicated in the pathogenesis of MS. |
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Formal Description Interaction-ID: 42742 |
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| Comment | CD4+ T helper cells (i.e.Th1, Th2, and Th17 cells) and CD8+ T cells have been shown to be present in MS lesions and are implicated in the pathogenesis of MS. |
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Formal Description Interaction-ID: 42752 |
tissue/cell line interacts (colocalizes) with phenotype multiple sclerosis lesion |
| Comment | CD4+ T helper cells (i.e.Th1, Th2, and Th17 cells) and CD8+ T cells have been shown to be present in MS lesions and are implicated in the pathogenesis of MS. |
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Formal Description Interaction-ID: 42759 |
tissue/cell line CD8+ T-lymphocyte interacts (colocalizes) with phenotype multiple sclerosis lesion |
| Comment | CD4+ T helper cells (i.e.Th1, Th2, and Th17 cells) and CD8+ T cells have been shown to be present in MS lesions and are implicated in the pathogenesis of MS. |
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Formal Description Interaction-ID: 42760 |
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| Comment | T cells have a key role in MS. There appears to be a dysregulation in levels or impairment of functioning of regulatory / anti-inflammatory T-cells in MS. |
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Formal Description Interaction-ID: 42761 |
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| Comment | B cells also appear to have a role in MS and demyelination as data have shown that B cells in the cerebrospinal fluid (CSF) correlate with early CNS inflammation in RRMS. |
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Formal Description Interaction-ID: 42770 |
phenotype affects_quantity of tissue/cell line |
| Comment | B cells also appear to have a role in MS and demyelination as data have shown that B cells in the cerebrospinal fluid (CSF) correlate with early CNS inflammation in RRMS. |
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Formal Description Interaction-ID: 42773 |
process affects_activity of phenotype |
| Comment | B-cells generate antibodies against myelin that activate the complement cascade, leading to opsonization (phagocytosis / destruction) of myelin and oligodendrocytes. |
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Formal Description Interaction-ID: 42776 |
tissue/cell line increases_activity of process |
| Comment | B-cells generate antibodies against myelin that activate the complement cascade, leading to opsonization (phagocytosis / destruction) of myelin and oligodendrocytes. |
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Formal Description Interaction-ID: 42780 |
tissue/cell line increases_activity of process |
| Comment | B-cells generate antibodies against myelin that activate the complement cascade, leading to opsonization (phagocytosis / destruction) of myelin and oligodendrocytes. |
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Formal Description Interaction-ID: 42783 |
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| Comment | B-cells generate antibodies against myelin that activate the complement cascade, leading to opsonization (phagocytosis / destruction) of myelin and oligodendrocytes. |
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Formal Description Interaction-ID: 42784 |
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| Comment | B-cells generate antibodies against myelin that activate the complement cascade, leading to opsonization (phagocytosis / destruction) of myelin and oligodendrocytes. |
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Formal Description Interaction-ID: 42785 |
process increases_activity of process |
| Comment | B-cells generate antibodies against myelin that activate the complement cascade, leading to opsonization (phagocytosis / destruction) of myelin and oligodendrocytes. |
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Formal Description Interaction-ID: 42786 |
process increases_activity of process |
| Comment | Memory B-cells (B-cell subtypes) stimulated CD4+ T-cell proliferation in response to neuro-antigens [myelin basic protein and myelin oligodendrocyte glycoprotein (MOG), a membrane protein expressed on oligodendrocytes in patients with RRMS]. |
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Formal Description Interaction-ID: 42788 |
tissue/cell line B-lymphocyte (memory subtype) increases_activity of process CD4+ T-cell proliferation |
| Comment | Certain B-cell subtypes (memory B-cells) contribute to proinflammatory cytokine production (e.g. lymphotoxin and TNF-alpha) and may act as antigen-presenting cells to activate T-cell differentiation. |
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Formal Description Interaction-ID: 42799 |
tissue/cell line B-lymphocyte (memory subtype) increases_quantity of gene/protein Proinflammatory cytokine |
| Comment | Certain B-cell subtypes (memory B-cells) contribute to proinflammatory cytokine production (e.g. lymphotoxin and TNF-alpha) and may act as antigen-presenting cells to activate T-cell differentiation. |
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Formal Description Interaction-ID: 42800 |
tissue/cell line B-lymphocyte (memory subtype) increases_quantity of gene/protein Lymphotoxin |
| Comment | Certain B-cell subtypes (memory B-cells) contribute to proinflammatory cytokine production (e.g. lymphotoxin and TNF-alpha) and may act as antigen-presenting cells to activate T-cell differentiation. |
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Formal Description Interaction-ID: 42801 |
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| Drugbank entries | Show/Hide entries for TNF |
| Comment | Certain B-cell subtypes (memory B-cells) contribute to proinflammatory cytokine production (e.g. lymphotoxin and TNF-alpha) and may act as antigen-presenting cells to activate T-cell differentiation. |
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Formal Description Interaction-ID: 42802 |
gene/protein Lymphotoxin affects_activity of gene/protein Proinflammatory cytokine |
| Comment | Some B-cells can exert anti-inflammatory effects through production of regulatory cytokines (e.g. IL-10) and facilitating T(reg)-cell (regulatory T-cells) development. |
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Formal Description Interaction-ID: 42846 |
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| Comment | Some B-cells can exert anti-inflammatory effects through production of regulatory cytokines (e.g. IL-10) and facilitating T(reg)-cell (regulatory T-cells) development. |
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Formal Description Interaction-ID: 42847 |
tissue/cell line affects_activity of |
| Comment | Some B-cells can exert anti-inflammatory effects through production of regulatory cytokines (e.g. IL-10) and facilitating T(reg)-cell (regulatory T-cells) development. |
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Formal Description Interaction-ID: 42848 |
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| Comment | Some B-cells can exert anti-inflammatory effects through production of regulatory cytokines (e.g. IL-10) and facilitating T(reg)-cell (regulatory T-cells) development. |
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Formal Description Interaction-ID: 42849 |
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| Comment | CD4+ Th2-cells produce IL-4, IL-5, and IL-13, that can inhibit macrophage function. |
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Formal Description Interaction-ID: 42850 |
tissue/cell line CD4+ Th2 helper cell increases_quantity of gene/protein |
| Comment | CD4+ Th2-cells produce IL-4, IL-5, and IL-13, that can inhibit macrophage function. |
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Formal Description Interaction-ID: 42851 |
tissue/cell line CD4+ Th2 helper cell increases_quantity of gene/protein |
| Drugbank entries | Show/Hide entries for IL5 |
| Comment | CD4+ Th2-cells produce IL-4, IL-5, and IL-13, that can inhibit macrophage function. |
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Formal Description Interaction-ID: 42852 |
tissue/cell line CD4+ Th2 helper cell increases_quantity of gene/protein |
| Comment | Astrocytes proliferate and become hypertrophic in new lesions and form glial scars in areas where axonal transection has occurred, which can be seen in chronic lesions. Astroglials carring impairs remyelination and repair. |
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Formal Description Interaction-ID: 42853 |
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| Comment | Astrocytes proliferate and become hypertrophic in new lesions and form glial scars in areas where axonal transection has occurred, which can be seen in chronic lesions. Astroglial scarring impairs remyelination and repair. |
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Formal Description Interaction-ID: 42858 |
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| Comment | Astrocytes proliferate and become hypertrophic in new lesions and form glial scars in areas where axonal transection has occurred, which can be seen in chronic lesions. Astroglial scarring impairs remyelination and repair. |
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Formal Description Interaction-ID: 42859 |
phenotype glial scar decreases_activity of process remyelination |
| Comment | Oligodendrocytes are damaged by inflammatory processes. Therefore remyelination is often incomplete. |
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Formal Description Interaction-ID: 42862 |
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| Comment | Axonal damage is seen early in MS lesion formation, suggesting that it may occur as a result of acute inflammatory demyelinating events, but acute axonal damage also occurs in partially remyelinating lesions and inactive demyelinated lesions. |
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Formal Description Interaction-ID: 42896 |
disease increases_activity of phenotype axonal damage |
| Comment | Some evidence shows that HPA axis function is dysregulated (HPA axis hyperactivity and chronic HPA activation) in patients with MS, although other data indicate normal HPA axis function. |
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Formal Description Interaction-ID: 42897 |
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| Comment | Impaired glucocorticoid receptor binding in lymphocytes may be a contributing factor to the suboptimal response in some MS patients to steroid treatment for relapses. |
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Formal Description Interaction-ID: 42898 |
disease affects_activity of process |
| Comment | Increased activity of HPA axis is also associated with fatigue and cognitive impairment, which are commonly reported by patients experiencing relapses. |
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Formal Description Interaction-ID: 42899 |
phenotype HPA axis hyperactivity increases_activity of phenotype |
| Comment | The extent of HPA axis hyperactivity is associated with the clinical type of MS, and may be a predictor of progression. |
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Formal Description Interaction-ID: 42900 |
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| Comment | Neurodegeneration has been linked to HPA axis hyperactivity. |
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Formal Description Interaction-ID: 42901 |
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| Comment | Increased activity of HPA axis is also associated with fatigue and cognitive impairment, which are commonly reported by patients experiencing relapses. |
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Formal Description Interaction-ID: 42902 |
phenotype HPA axis hyperactivity increases_activity of phenotype cognitive impairment |
| Comment | High-dose corticosteroids are the standard of care for treating MS relapses. Adverse events associated with high-dose corticosteroids include infection, hyperglycemia, mood effects (euphoria, psychosis), gastrointestinal symptoms, taste disturbances, insomnia, weight gain, edema, and hypertension; potential long-term effects include osteoporosis, cataracts, glaucoma, Cushingoid features, immune suppression, hypernatremia, and hypokalemia; rarely, patients treated with corticosteroids may develop avascular necrosis (AVN) of major joints, even after one dose of corticosteroid. |
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Formal Description Interaction-ID: 42903 |
drug/chemical compound Corticosteroid increases_activity of process infection |
| Comment | High-dose corticosteroids are the standard of care for treating MS relapses. Adverse events associated with high-dose corticosteroids include infection, hyperglycemia, mood effects (euphoria, psychosis), gastrointestinal symptoms, taste disturbances, insomnia, weight gain, edema, and hypertension; potential long-term effects include osteoporosis, cataracts, glaucoma, Cushingoid features, immune suppression, hypernatremia, and hypokalemia; rarely, patients treated with corticosteroids may develop avascular necrosis (AVN) of major joints, even after one dose of corticosteroid. |
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Formal Description Interaction-ID: 42908 |
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| Comment | High-dose corticosteroids are the standard of care for treating MS relapses. Adverse events associated with high-dose corticosteroids include infection, hyperglycemia, mood effects (euphoria, psychosis), gastrointestinal symptoms, taste disturbances, insomnia, weight gain, edema, and hypertension; potential long-term effects include osteoporosis, cataracts, glaucoma, Cushingoid features, immune suppression, hypernatremia, and hypokalemia; rarely, patients treated with corticosteroids may develop avascular necrosis (AVN) of major joints, even after one dose of corticosteroid. |
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Formal Description Interaction-ID: 42909 |
drug/chemical compound Corticosteroid increases_activity of phenotype psychosis |
| Comment | High-dose corticosteroids are the standard of care for treating MS relapses. Adverse events associated with high-dose corticosteroids include infection, hyperglycemia, mood effects (euphoria, psychosis), gastrointestinal symptoms, taste disturbances, insomnia, weight gain, edema, and hypertension; potential long-term effects include osteoporosis, cataracts, glaucoma, Cushingoid features, immune suppression, hypernatremia, and hypokalemia; rarely, patients treated with corticosteroids may develop avascular necrosis (AVN) of major joints, even after one dose of corticosteroid. |
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Formal Description Interaction-ID: 42910 |
drug/chemical compound Corticosteroid increases_activity of phenotype euphoria |
| Comment | High-dose corticosteroids are the standard of care for treating MS relapses. Adverse events associated with high-dose corticosteroids include infection, hyperglycemia, mood effects (euphoria, psychosis), gastrointestinal symptoms, taste disturbances, insomnia, weight gain, edema, and hypertension; potential long-term effects include osteoporosis, cataracts, glaucoma, Cushingoid features, immune suppression, hypernatremia, and hypokalemia; rarely, patients treated with corticosteroids may develop avascular necrosis (AVN) of major joints, even after one dose of corticosteroid. |
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Formal Description Interaction-ID: 42911 |
drug/chemical compound Corticosteroid increases_activity of phenotype gastrointestinal dysfunction |
| Comment | High-dose corticosteroids are the standard of care for treating MS relapses. Adverse events associated with high-dose corticosteroids include infection, hyperglycemia, mood effects (euphoria, psychosis), gastrointestinal symptoms, taste disturbances, insomnia, weight gain, edema, and hypertension; potential long-term effects include osteoporosis, cataracts, glaucoma, Cushingoid features, immune suppression, hypernatremia, and hypokalemia; rarely, patients treated with corticosteroids may develop avascular necrosis (AVN) of major joints, even after one dose of corticosteroid. |
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Formal Description Interaction-ID: 42912 |
drug/chemical compound Corticosteroid increases_activity of phenotype taste disturbance |
| Comment | High-dose corticosteroids are the standard of care for treating MS relapses. Adverse events associated with high-dose corticosteroids include infection, hyperglycemia, mood effects (euphoria, psychosis), gastrointestinal symptoms, taste disturbances, insomnia, weight gain, edema, and hypertension; potential long-term effects include osteoporosis, cataracts, glaucoma, Cushingoid features, immune suppression, hypernatremia, and hypokalemia; rarely, patients treated with corticosteroids may develop avascular necrosis (AVN) of major joints, even after one dose of corticosteroid. |
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Formal Description Interaction-ID: 42913 |
drug/chemical compound Corticosteroid increases_activity of phenotype insomnia |
| Comment | High-dose corticosteroids are the standard of care for treating MS relapses. Adverse events associated with high-dose corticosteroids include infection, hyperglycemia, mood effects (euphoria, psychosis), gastrointestinal symptoms, taste disturbances, insomnia, weight gain, edema, and hypertension; potential long-term effects include osteoporosis, cataracts, glaucoma, Cushingoid features, immune suppression, hypernatremia, and hypokalemia; rarely, patients treated with corticosteroids may develop avascular necrosis (AVN) of major joints, even after one dose of corticosteroid. |
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Formal Description Interaction-ID: 42914 |
drug/chemical compound Corticosteroid increases_activity of phenotype |
| Comment | High-dose corticosteroids are the standard of care for treating MS relapses. Adverse events associated with high-dose corticosteroids include infection, hyperglycemia, mood effects (euphoria, psychosis), gastrointestinal symptoms, taste disturbances, insomnia, weight gain, edema, and hypertension; potential long-term effects include osteoporosis, cataracts, glaucoma, Cushingoid features, immune suppression, hypernatremia, and hypokalemia; rarely, patients treated with corticosteroids may develop avascular necrosis (AVN) of major joints, even after one dose of corticosteroid. |
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Formal Description Interaction-ID: 42915 |
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| Comment | High-dose corticosteroids are the standard of care for treating MS relapses. Adverse events associated with high-dose corticosteroids include infection, hyperglycemia, mood effects (euphoria, psychosis), gastrointestinal symptoms, taste disturbances, insomnia, weight gain, edema, and hypertension; potential long-term effects include osteoporosis, cataracts, glaucoma, Cushingoid features, immune suppression, hypernatremia, and hypokalemia; rarely, patients treated with corticosteroids may develop avascular necrosis (AVN) of major joints, even after one dose of corticosteroid. |
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Formal Description Interaction-ID: 42916 |
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| Comment | High-dose corticosteroids are the standard of care for treating MS relapses. Adverse events associated with high-dose corticosteroids include infection, hyperglycemia, mood effects (euphoria, psychosis), gastrointestinal symptoms, taste disturbances, insomnia, weight gain, edema, and hypertension; potential long-term effects include osteoporosis, cataracts, glaucoma, Cushingoid features, immune suppression, hypernatremia, and hypokalemia; rarely, patients treated with corticosteroids may develop avascular necrosis (AVN) of major joints, even after one dose of corticosteroid. |
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Formal Description Interaction-ID: 42917 |
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| Comment | High-dose corticosteroids are the standard of care for treating MS relapses. Adverse events associated with high-dose corticosteroids include infection, hyperglycemia, mood effects (euphoria, psychosis), gastrointestinal symptoms, taste disturbances, insomnia, weight gain, edema, and hypertension; potential long-term effects include osteoporosis, cataracts, glaucoma, Cushingoid features, immune suppression, hypernatremia, and hypokalemia; rarely, patients treated with corticosteroids may develop avascular necrosis (AVN) of major joints, even after one dose of corticosteroid. |
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Formal Description Interaction-ID: 42918 |
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| Comment | High-dose corticosteroids are the standard of care for treating MS relapses. Adverse events associated with high-dose corticosteroids include infection, hyperglycemia, mood effects (euphoria, psychosis), gastrointestinal symptoms, taste disturbances, insomnia, weight gain, edema, and hypertension; potential long-term effects include osteoporosis, cataracts, glaucoma, Cushingoid features, immune suppression, hypernatremia, and hypokalemia; rarely, patients treated with corticosteroids may develop avascular necrosis (AVN) of major joints, even after one dose of corticosteroid. |
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Formal Description Interaction-ID: 42919 |
drug/chemical compound Corticosteroid increases_activity of disease Glaucoma |
| Comment | High-dose corticosteroids are the standard of care for treating MS relapses. Adverse events associated with high-dose corticosteroids include infection, hyperglycemia, mood effects (euphoria, psychosis), gastrointestinal symptoms, taste disturbances, insomnia, weight gain, edema, and hypertension; potential long-term effects include osteoporosis, cataracts, glaucoma, Cushingoid features, immune suppression, hypernatremia, and hypokalemia; rarely, patients treated with corticosteroids may develop avascular necrosis (AVN) of major joints, even after one dose of corticosteroid. |
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Formal Description Interaction-ID: 42920 |
drug/chemical compound Corticosteroid increases_activity of phenotype Cushingoid features |
| Comment | High-dose corticosteroids are the standard of care for treating MS relapses. Adverse events associated with high-dose corticosteroids include infection, hyperglycemia, mood effects (euphoria, psychosis), gastrointestinal symptoms, taste disturbances, insomnia, weight gain, edema, and hypertension; potential long-term effects include osteoporosis, cataracts, glaucoma, Cushingoid features, immune suppression, hypernatremia, and hypokalemia; rarely, patients treated with corticosteroids may develop avascular necrosis (AVN) of major joints, even after one dose of corticosteroid. |
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Formal Description Interaction-ID: 42938 |
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| Comment | High-dose corticosteroids are the standard of care for treating MS relapses. Adverse events associated with high-dose corticosteroids include infection, hyperglycemia, mood effects (euphoria, psychosis), gastrointestinal symptoms, taste disturbances, insomnia, weight gain, edema, and hypertension; potential long-term effects include osteoporosis, cataracts, glaucoma, Cushingoid features, immune suppression, hypernatremia, and hypokalemia; rarely, patients treated with corticosteroids may develop avascular necrosis (AVN) of major joints, even after one dose of corticosteroid. |
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Formal Description Interaction-ID: 42939 |
drug/chemical compound Corticosteroid increases_activity of phenotype |
| Comment | High-dose corticosteroids are the standard of care for treating MS relapses. Adverse events associated with high-dose corticosteroids include infection, hyperglycemia, mood effects (euphoria, psychosis), gastrointestinal symptoms, taste disturbances, insomnia, weight gain, edema, and hypertension; potential long-term effects include osteoporosis, cataracts, glaucoma, Cushingoid features, immune suppression, hypernatremia, and hypokalemia; rarely, patients treated with corticosteroids may develop avascular necrosis (AVN) of major joints, even after one dose of corticosteroid. |
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Formal Description Interaction-ID: 42940 |
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| Comment | High-dose corticosteroids are the standard of care for treating MS relapses. Adverse events associated with high-dose corticosteroids include infection, hyperglycemia, mood effects (euphoria, psychosis), gastrointestinal symptoms, taste disturbances, insomnia, weight gain, edema, and hypertension; potential long-term effects include osteoporosis, cataracts, glaucoma, Cushingoid features, immune suppression, hypernatremia, and hypokalemia; rarely, patients treated with corticosteroids may develop avascular necrosis (AVN) of major joints, even after one dose of corticosteroid. |
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Formal Description Interaction-ID: 42941 |
drug/chemical compound Corticosteroid increases_activity of phenotype avascular necrosis |
| Comment | The side effect profile of ACTH is generally similar to that of corticosteroids, and includes fluid retention, alteration in glucose tolerance, elevation in blood pressure, behavioral and mood changes, increased appetite, and weight gain; ACTH may have milder effects on bone and less risk of AVN. |
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Formal Description Interaction-ID: 42942 |
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| Drugbank entries | Show/Hide entries for Corticotropin |
| Comment | The side effect profile of ACTH is generally similar to that of corticosteroids, and includes fluid retention, alteration in glucose tolerance, elevation in blood pressure, behavioral and mood changes, increased appetite, and weight gain; ACTH may have milder effects on bone and less risk of AVN. |
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Formal Description Interaction-ID: 42943 |
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| Drugbank entries | Show/Hide entries for Corticotropin |
| Comment | The side effect profile of ACTH is generally similar to that of corticosteroids, and includes fluid retention, alteration in glucose tolerance, elevation in blood pressure, behavioral and mood changes, increased appetite, and weight gain; ACTH may have milder effects on bone and less risk of AVN. |
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Formal Description Interaction-ID: 42944 |
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| Drugbank entries | Show/Hide entries for Corticotropin |
| Comment | The side effect profile of ACTH is generally similar to that of corticosteroids, and includes fluid retention, alteration in glucose tolerance, elevation in blood pressure, behavioral and mood changes, increased appetite, and weight gain; ACTH may have milder effects on bone and less risk of AVN. |
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Formal Description Interaction-ID: 42945 |
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| Drugbank entries | Show/Hide entries for Corticotropin |
| Comment | The side effect profile of ACTH is generally similar to that of corticosteroids, and includes fluid retention, alteration in glucose tolerance, elevation in blood pressure, behavioral and mood changes, increased appetite, and weight gain; ACTH may have milder effects on bone and less risk of AVN. |
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Formal Description Interaction-ID: 42946 |
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| Drugbank entries | Show/Hide entries for Corticotropin |
| Comment | The side effect profile of ACTH is generally similar to that of corticosteroids, and includes fluid retention, alteration in glucose tolerance, elevation in blood pressure, behavioral and mood changes, increased appetite, and weight gain; ACTH may have milder effects on bone and less risk of AVN. |
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Formal Description Interaction-ID: 42947 |
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| Drugbank entries | Show/Hide entries for Corticotropin |
| Comment | The side effect profile of ACTH is generally similar to that of corticosteroids, and includes fluid retention, alteration in glucose tolerance, elevation in blood pressure, behavioral and mood changes, increased appetite, and weight gain; ACTH may have milder effects on bone and less risk of AVN. |
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Formal Description Interaction-ID: 42948 |
drug/chemical compound increases_activity of phenotype |
| Drugbank entries | Show/Hide entries for Corticotropin |
| Comment | In studies on experimental autoimmune encephalomyelitis (EAE, a mouse model for MS), orally administered ACTH induced expression of T(reg) cells, increased secretion of immunoregulatory IL-4, and decreased IL-17, IL-2, and IFN-gamma in CNS lymphocytes, while alpha-MSH induced T-cells to produce regulatory cytokines. |
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Formal Description Interaction-ID: 42954 |
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| Comment | In studies on experimental autoimmune encephalomyelitis (EAE, a mouse model for MS), orally administered ACTH induced expression of T(reg) cells, increased secretion of immunoregulatory IL-4, and decreased IL-17, IL-2, and IFN-gamma in CNS lymphocytes, while alpha-MSH induced T-cells to produce regulatory cytokines. |
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Formal Description Interaction-ID: 42961 |
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| Comment | In studies on experimental autoimmune encephalomyelitis (EAE, a mouse model for MS), orally administered ACTH induced expression of T(reg) cells, increased secretion of immunoregulatory IL-4, and decreased IL-17, IL-2, and IFN-gamma in CNS lymphocytes, while alpha-MSH induced T-cells to produce regulatory cytokines. |
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Formal Description Interaction-ID: 42963 |
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| Comment | In studies on experimental autoimmune encephalomyelitis (EAE, a mouse model for MS), orally administered ACTH induced expression of T(reg) cells, increased secretion of immunoregulatory IL-4, and decreased IL-17, IL-2, and IFN-gamma in CNS lymphocytes, while alpha-MSH induced T-cells to produce regulatory cytokines. |
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Formal Description Interaction-ID: 42965 |
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| Drugbank entries | Show/Hide entries for IL2 |
| Comment | In studies on experimental autoimmune encephalomyelitis (EAE, a mouse model for MS), orally administered ACTH induced expression of T(reg) cells, increased secretion of immunoregulatory IL-4, and decreased IL-17, IL-2, and IFN-gamma in CNS lymphocytes, while alpha-MSH induced T-cells to produce regulatory cytokines. |
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Formal Description Interaction-ID: 42967 |
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| Drugbank entries | Show/Hide entries for IFNG |
| Comment | In studies on experimental autoimmune encephalomyelitis (EAE, a mouse model for MS), orally administered ACTH induced expression of T(reg) cells, increased secretion of immunoregulatory IL-4, and decreased IL-17, IL-2, and IFN-gamma in CNS lymphocytes, while alpha-MSH induced T-cells to produce regulatory cytokines. |
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Formal Description Interaction-ID: 42968 |
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| Comment | In studies on experimental autoimmune encephalomyelitis (EAE, a mouse model for MS), orally administered ACTH induced expression of T(reg) cells, increased secretion of immunoregulatory IL-4, and decreased IL-17, IL-2, and IFN-gamma in CNS lymphocytes, while alpha-MSH induced T-cells to produce regulatory cytokines. |
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Formal Description Interaction-ID: 42969 |
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| Comment | Studies of experimental autoimmune uveitis have shown that alpha-MSH mediates the induction of T(reg)-cells and modulates T-cell phenotype, essentially converting primed T-cells to act as T(reg)-cells. |
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Formal Description Interaction-ID: 42970 |
gene/protein increases_activity of tissue/cell line |
| Comment | Studies of experimental autoimmune uveitis have shown that alpha-MSH mediates the induction of T(reg)-cells and modulates T-cell phenotype, essentially converting primed T-cells to act as T(reg)-cells. |
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Formal Description Interaction-ID: 42971 |
gene/protein increases_activity of |
| Comment | One study found that add-on treatment with albuterol in MS patients receiving glatiramer acetate was associated with improvement in clinical outcomes, including relapse rates, and MS Functional Composite (MSFC) scores at 6 and 12 months. |
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Formal Description Interaction-ID: 42972 |
drug/chemical compound decreases_activity of disease |
| Comment | ACTH modulates synthesis, release, and actions of neurotransmitters, including dopamine and acetylcholine, within the CNS. |
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Formal Description Interaction-ID: 42973 |
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| Comment | ACTH modulates synthesis, release, and actions of neurotransmitters, including dopamine and acetylcholine, within the CNS. |
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Formal Description Interaction-ID: 42974 |
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| Comment | ACTH modulates synthesis, release, and actions of neurotransmitters, including dopamine and acetylcholine, within the CNS. |
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Formal Description Interaction-ID: 42975 |
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| Drugbank entries | Show/Hide entries for |
| Comment | ACTH modulates synthesis, release, and actions of neurotransmitters, including dopamine and acetylcholine, within the CNS. |
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Formal Description Interaction-ID: 42976 |
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| Comment | ACTH modulates synthesis, release, and actions of neurotransmitters, including dopamine and acetylcholine, within the CNS. |
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Formal Description Interaction-ID: 42977 |
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| Comment | ACTH modulates synthesis, release, and actions of neurotransmitters, including dopamine and acetylcholine, within the CNS. |
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Formal Description Interaction-ID: 42978 |
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| Drugbank entries | Show/Hide entries for |
| Comment | ACTH modulates synthesis, release, and actions of neurotransmitters, including dopamine and acetylcholine, within the CNS. |
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Formal Description Interaction-ID: 42979 |
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| Comment | ACTH modulates synthesis, release, and actions of neurotransmitters, including dopamine and acetylcholine, within the CNS. |
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Formal Description Interaction-ID: 42980 |
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