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.
|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%|
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.
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.
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.
Regulation of T cell activation by Notch ligand, DLL4
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).
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