Upload at 2018-04-03 15:19:07
Causal Biological Networks Database
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.
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Number Nodes
Number Edges
Number Components
Network Density
Average Degree
Number Citations
Number BEL Errors

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


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


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


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


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