Table 3.
Dataset | Pathway name | Rank | Description | Ref |
---|---|---|---|---|
H5N1 | JAK-STAT signaling pathway | 3→2 | The challenging respiratory epithelial cells with hemagglutinin of H5N1 exploit the JAK2/3/STAT1 and result in a large release of cytokines, initiating a destructive innate immune response. | [36] |
PI3k-Akt signaling pathway | 6→5 | PI3K-Akt signaling, which can be activated by the NS1 protein of H5N1, is crucial for viral replication. | [43] | |
Apoptosis | 139→31 | Apoptosis plays a major role in the pathogenesis of H5N1 virus in humans by destroying alveolar epithelial cells. | [44] | |
Th17 | Cytokine-cytokine receptor interaction | 33→10 | The differentiation of T H17 cells from naive CD4 + T cells is regulated by multiple cytokines. | [38] |
MAPK signaling pathway | 47→40 | MAPKs play a supplemental role in mediating the intracellular responses to TGF- β required for differentiation of T H17. | [39] | |
Toll-like receptor signaling pathway | 46→41 | Differentiation of T H17 cell is induced by proinflammatory cytokines generated by ligation of a subset of toll-like receptors. | [41] |
It represents part of the pathways from H5N1 and Th17 that rank higher in ContextTRAP than in original TRAP. Rank column shows how the rank of the pathway in original TRAP is changed in ContextTRAP. Relation between those pathways and the context of the dataset is described with reference