Provenance

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charles.hoyt@scai.fraunhofer.de at 2018-04-03 15:19:07
Authors
Causal Biological Networks Database
Contact
CausalBiologicalNetworks.RD@pmi.com
Description
The Th17 Signaling network depicts the causal mechanisms that are activated in IL-17-producing T helper (Th17) cells following T-cell receptor (TCR) ligation. Expanding on these processes, the network highlights the chemokines secreted by macrophages and dendritic cells, as well as the cognate T-cell receptors, involved in mediating T-cell recruitment to compromised lung tissue during COPD development.
License
Please cite: - www.causalbionet.com - https://bionet.sbvimprover.com as well as any relevant publications. The sbv IMPROVER project, the website and the Symposia are part of a collaborative project designed to enable scientists to learn about and contribute to the development of a new crowd sourcing method for verification of scientific data and results. The current challenges, website and biological network models were developed and are maintained as part of a collaboration among Selventa, OrangeBus and ADS. The project is led and funded by Philip Morris International. For more information on the focus of Philip Morris International’s research, please visit www.pmi.com.
Number Nodes
65
Number Edges
118
Number Components
11
Network Density
0.0283654
Average Degree
1.81538
Number Citations
73
Number BEL Errors
0

Content Statistics

Network Overlap

The node-based overlap between this network and other networks is calculated as the Szymkiewicz-Simpson coefficient of their respective nodes. Up to the top 10 are shown below.

Network Overlap
Th1-Th2 Signaling-2.0-Rn v2.0 51%
Cytotoxic T-cell Signaling-2.0-Rn v2.0 45%
Dendritic Cell Signaling-2.0-Rn v2.0 43%
Treg Signaling-2.0-Rn v2.0 42%
BEL Framework Large Corpus Document v20170611 40%
Selventa Protein Families Definitions v20150611 28%
NK Signaling-2.0-Rn v2.0 25%
Th17 Signaling-2.0-Hs v2.0 23%
Th17 Signaling-2.0-Mm v2.0 22%
Immune Regulation of Tissue Repair-2.0-Rn v2.0 18%

Sample Edges

p(HGNC:IL26) increases path(SDIS:"T-helper 17 cell activation")

Upon culture with IL-26-stimulated monocytes, IL-23R− and CCR6− CD161− memory T cells acquired the ability to secrete IL-17A (Figure 7C), demonstrating that IL-26 favors Th17 cell generation by inducing non-Th17-committed memory T cell differentiation into Th17 cells. Other:23055831

a(SCHEM:Imiquimod) increases bp(GOBP:"inflammatory response")

In summary, to our knowledge, we are the first to demonstrate that RORγt inverse agonists: 1) inhibit Tc17 cell differentiation, as well as IL-17 production by γδ T cells and CD8+ Tc17 cells; 2) block imiquimod-induced cutaneous inflammation; 3) inhibit Th17 signature gene expression by cells isolated from psoriatic patient samples; and 4) block IL-23-induced IL-17A expression. Other:24516202

p(RGD:Dll4) increases act(p(SFAM:"NOTCH Family"), ma(tscript))

In the present study, we show that VEGF-induced DLL4 expression depends on NOTCH activation. VEGF-induced DLL4 expression was prevented by the blockage of NOTCH signaling with ??-secretase or ADAM inhibitors in human cardiac microvascular ECs. Similar to VEGF-A, recombinant DLL4 itself stimulated NOTCH signaling and resulted in up-regulation of DLL4, suggesting a positive feed-forward mechanism. PubMed:20959466

p(RGD:Dll4) increases act(p(SFAM:"NOTCH Family"), ma(tscript))

Regulation of T cell activation by Notch ligand, DLL4 PubMed:19494260

act(p(RGD:Tgfbr2), ma(kin)) directlyIncreases act(p(RGD:Tgfbr1), ma(kin))

These proteins signal by stimulating formation of specific heteromeric complexes of type I and type II serine/threonine kinase receptors. The type II receptors are encoded by five known mammalian genes, bind to ligands, and phosphorylate and activate the type I receptors, of which there are seven mammalian members (Fig. 1). PubMed:11792802

Sample Nodes

p(RGD:Ccl3)

In-Edges: 11 | Out-Edges: 19 | Explore Neighborhood | Download JSON

bp(GOBP:"inflammatory response")

In-Edges: 792 | Out-Edges: 404 | Children: 3 | Explore Neighborhood | Download JSON

p(RGD:Ifng)

In-Edges: 45 | Out-Edges: 79 | Explore Neighborhood | Download JSON

p(RGD:Il6)

In-Edges: 166 | Out-Edges: 99 | Explore Neighborhood | Download JSON

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 the open source project, PyBEL. Please feel free to contact us here to give us feedback or report any issues.