TABLE 1.
Unique genes from Venn diagram analysis of HT-29 cells challenged with poly(I·C) only and PC only in descending order of fold change in expressiona
Challenge (no. of unique genes), immune gene protein | Function | Immune pathway(s) | Fold change in expressionb |
---|---|---|---|
Poly(I·C) only (n = 37) | |||
IL-17C (cytokine) | T cell-derived cytokine that stimulates the release of TNF-α and IL-1β | Inflammatory cytokine and receptors | 12.41 |
LTB (cytokine) | Cytokine with a specific role in immune response regulation | Cytokine-cytokine receptor interaction | 8.20 |
TNF-α (cytokine) | Potent proinflammatory cytokine, involved in inflammatory responses | MAPK signaling pathway, TGF-β signaling pathway, cytokine-cytokine receptor interaction | 6.77 |
CSF2 (cytokine) | Cytokine that stimulates growth and differentiation | JAK-STAT signaling, cytokine-cytokine receptor interaction, T cell receptor signaling | 6.31 |
NF-κB2 | Pleiotropic transcription factor involved in inflammation, immunity, differentiation, cell growth, tumorigenesis, and apoptosis | MAPK signaling pathway, NF-κB signaling pathway | 5.32 |
CDKN1A | Intermediate inhibitor of cellular proliferation in response to DNA damage | p53 signaling, cell cycle | 4.72 |
CSF1 (cytokine) | Granulocyte-macrophage colony-stimulating factors that have a role in immune defenses | Cytokine-cytokine receptor interaction | 4.14 |
IRF1 | Transcriptional activator for IFN-α-, IFN-β-, and IFN-γ-stimulated genes, a modulator of virus-induced signaling | NF-κB signaling pathway, TLR signaling pathway | 3.86 |
BMP2 | Member of the TGF-β superfamily | TGF-β signaling pathway, cytokine-cytokine receptor interaction | 3.77 |
RELB | Component of the NF-κB RelB-p52 complex | MAPK signaling pathway, NF-κB signaling pathway | 3.38 |
BF | Not in Gene Cards database | No pathway | 3.17 |
IL-32 (cytokine) | Inducer of TNF-α and IL-8, activating cytokine signaling pathways of NF-κB and p38 MAPK | Inflammatory response and autoimmunity | 3.04 |
OASL | Binder to double-stranded RNA and DNA | No KEGG pathway | 2.95 |
IFNGR2 | Accessory factor of the IFN-γ signal transduction pathway | Cytokine-cytokine receptor interaction | 2.93 |
TNFRSF12A | Inducer of apoptosis in some cell types | Cytokine-cytokine receptor interaction, NF-κB signaling pathway, apoptosis | 2.89 |
ICAM1 | Adhesion molecule, intercellular 1, upregulated by cytokines | CAMs | 2.80 |
ELF3 | Transcriptional activator that binds and transactivates external transcribed spacer (ETS) sequences | Selected targets of ESR1 | 2.74 |
ISG20 | Exonuclease involved in the antiviral function of IFN against RNA viruses | IFN-α and IFN-β response | 2.59 |
IL-28B (cytokine) | Protein with immunomodulatory activity that displays potent antiviral activity | Cytokine-cytokine receptor interaction, JAK-STAT signaling pathway | 2.52 |
MAP2K3 | Mitogen-activated protein kinase 3, critical component of TNF signaling | MAPK signaling pathway, TLR signaling pathway | 2.48 |
NR4A1 | Regulator of expression of delayed-early genes during liver regeneration | MAPK signaling pathway | 2.43 |
VEGF | Signaling protein involved in angiogenesis | Cytokine-cytokine receptor interaction | 2.39 |
IFIT2 | IFN-α-inducible protein induced by viral infections | Interferons and receptors | 2.38 |
JUNB | Transcription factor involved in regulating primary growth factor response | MAPK signaling pathway, JAK-STAT signaling pathway | 2.36 |
BCL2L1 | Potent inhibitor of cell death, regulating cell death by blocking the voltage-dependent anion channel (VDAC) | Apoptosis, JAK-STAT signaling pathway | 2.36 |
IL-29 (cytokine) | Protein involved in antiviral immunity and induced by viral infections or dsRNA | Cytokine-cytokine receptor interaction, JAK-STAT signaling pathway | 2.35 |
STAT5A | Protein involved in signal transduction and activation of transcription in response to cytokines | JAK-STAT signaling pathway | 2.35 |
TRIF | Adaptor used by TLR3 and TL4R to mediate NF-κB and interferon-regulatory factor (IRF) activation | NF-κB signaling, TLR signaling pathway | 2.26 |
MAP3K11 | Kinase that activates MAPK8/JNK kinase and functions as a positive regulator of the Jun N-terminal protein kinase signaling pathway | MAPK signaling pathway | 2.25 |
NFKB1 | Rapidly acting primary transcription factor that plays a key role in regulating the immune response to infection | MAPK signaling pathway, NF-κB signaling pathway | 2.20 |
CLCF1 (cytokine) | Cytokine with a B cell-stimulating capability | Cytokine-cytokine receptor interaction, JAK-STAT signaling pathway | 2.20 |
GBP1 | Guanylate binding protein mediating an antiviral response | JAK-STAT signaling pathway | 2.20 |
DUSP5 | Phosphatase that inactivates members of the MAPK superfamily | MAPK signaling pathway | 2.15 |
IKBKE | Noncanonical IκB kinase (IKK) that is essential for regulating antiviral signaling pathways | NF-κB signaling pathway, TLR signaling pathway | 2.14 |
RGS3 | Downregulator of G-protein-mediated release of inositol phosphates and activation of MAPKs | G-protein signaling, G-protein alpha-q signaling cascades | 2.05 |
CXCL11 (chemokine) | Chemotactic protein for interleukin-activated T cells | Cytokine-cytokine receptor interaction, chemokine signaling pathway, TLR signaling pathway | 2.04 |
GCH1 | Member of the GTP cyclohydrolase family in BH4 biosynthesis | Nitric oxide signaling pathway, neurotransmitter receptors/regulators, IFN-α and IFN-β response | 2.03 |
PC only (n = 3) | |||
IFITM1 | IFN-induced antiviral protein that mediates cellular innate immunity | Interferon signaling pathway, B cell receptor signaling pathway | 2.36 |
FGF19 | Protein involved in the suppression of bile acid biosynthesis | MAPK signaling pathway | 2.20 |
IFI44L | Member of the IFI44 family | Interferons and receptors pathway | 2.10 |
Immune gene function data are from GeneCards (http://www.genecards.org), and immune pathway data are from KEGG (http://www.genome.jp/kegg/pathway.html).
All genes were upregulated. Fold change or expression ratio = 2log2ratio. A 2-fold change in differentially expressed genes and a P value of <0.05 were considered statistically significant.