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a(MESH:Macrophages)

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Entity

Name
Macrophages
Namespace
mesh
Namespace Version
20180828
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/1b20f0637c395f8aa89c2e2e342d7b704062c242/external/mesh-names.belns

Appears in Networks 3

Functional aspects of meningeal lymphatics in ageing and Alzheimer’s disease v1.0.0

Nuclear receptors as therapeutic targets for Alzheimer's disease. v1.0.0

Amelioration of Experimental Autoimmune Encephalomyelitis by Anatabine v1.0.0

In-Edges 6

a(CHEBI:"amyloid-beta") association a(MESH:Macrophages) View Subject | View Object

Macrophages in the dura of cases with Alzheimer’s disease were also found in close proximity to amyloid-β deposits (Fig. 3l) PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Dura Mater
MeSH
Alzheimer Disease

act(a(MESH:"Lymphatic Vessels")) decreases a(MESH:Macrophages) View Subject | View Object

Analysis of lymphoid and myeloid cell populations in the meninges (Extended Data Fig. 9d) demonstrated a significant increase in the number of macrophages upon lymphatic ablation compared to both control groups (Extended Data Fig. 9e), which might be correlated with increased amyloid-β deposition and inflammation in the meninges PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

a(MESH:Glucocorticoids) decreases a(MESH:Macrophages) View Subject | View Object

The M2c macrophages are thought to be in an ‘acquired deactivation’ state induced by IL-10, TGF-b, glucocorticoids or contact with apoptotic cells, and are associated with a suppression of the innate immune response. PubMed:21718217

Appears in Networks:
Annotations
Confidence
Medium

p(HGNC:IL10) decreases a(MESH:Macrophages) View Subject | View Object

The M2c macrophages are thought to be in an ‘acquired deactivation’ state induced by IL-10, TGF-b, glucocorticoids or contact with apoptotic cells, and are associated with a suppression of the innate immune response. PubMed:21718217

Appears in Networks:
Annotations
Confidence
Medium

p(HGNC:TGFB1) decreases a(MESH:Macrophages) View Subject | View Object

The M2c macrophages are thought to be in an ‘acquired deactivation’ state induced by IL-10, TGF-b, glucocorticoids or contact with apoptotic cells, and are associated with a suppression of the innate immune response. PubMed:21718217

Appears in Networks:
Annotations
Confidence
Medium

a(CHEBI:Anatabine) decreases tloc(a(MESH:Macrophages), fromLoc(GO:"extracellular region"), toLoc(MESH:"Spinal Cord")) View Subject | View Object

In addition, anatabine markedly decreased the Iba1 immunostaining in the spinal cord of EAE mice showing that anatabine reduces the infiltration of macrophage/ microglia in the spinal cord of EAE mice (Fig. 10) PubMed:23383175

Appears in Networks:
Annotations
MeSH
Spinal Cord
MeSH
Encephalomyelitis

Out-Edges 2

a(MESH:Macrophages) regulates deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

By contrast, the parenchyma of the CNS is devoid of lymphatic vasculature2; in the brain, removal of cellular debris and toxic molecules, such as amyloid-β peptides, is mediated by a combination of transcellular transport mechanisms across the blood−brain and blood−cerebrospinal fluid (CSF) barriers7–9, phagocytosis and digestion by resident microglia and recruited monocytes and/or macrophages10,11, as well as CSF influx and ISF efflux through a paravascular (glymphatic) route12–14 PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain

a(MESH:Macrophages) association a(CHEBI:"amyloid-beta") View Subject | View Object

Macrophages in the dura of cases with Alzheimer’s disease were also found in close proximity to amyloid-β deposits (Fig. 3l) PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Dura Mater
MeSH
Alzheimer Disease

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.