Type I Interferon
Gene co-expression module in Monocytes
| Category | Antiviral |
|---|---|
| Genes | 10 |
| Annotation certainty | 5 of 5 |
| Annotation consistency | 9 of 10 genes have a known function matching the annotation |
Why this annotation
All top hub genes are canonical type I interferon-stimulated genes (ISGs): RSAD2 (viperin), IFIT1, IFIT2, IFIT3, CMPK2, USP18, HERC5, and OASL are among the most well-characterized ISGs induced by IFN-alpha/beta signaling. USP18 is a key negative regulator of the JAK-STAT/IFN pathway. OPTN (optineurin) participates in antiviral innate immune signaling. DEFB1 is a defensin with antiviral/antimicrobial roles but is a peripheral member here. The module is core coherent, uniformly expressed across subsets (consistent with a systemic IFN response rather than a subset-specific program), and shows low mean expression/pct positive consistent with a minority of cells in an activated antiviral state. The disease association (elevated in inflammation, reduced in remission) is consistent with IFN-driven inflammation in IBD. This is a classic type I interferon response module.
Genes
CMPK2, DEFB1, HERC5, IFIT1, IFIT2, IFIT3, OASL, OPTN, RSAD2, USP18
Most correlated modules
- Type I Interferon Response · correlation 0.92
- IFN-gamma Response · correlation 0.88
- JAK-STAT IFN Signaling · correlation 0.80
- Monocyte Chemokine Secretion · correlation 0.78
- Inflammasome Activation · correlation 0.72
- Immunoproteasome Antigen Processing · correlation 0.65
- Inflammatory Monocyte Activation · correlation 0.56
Module annotations were drafted by a large language model from the module's genes, then reviewed and approved by a domain expert. See sources & licences.