Type I Interferon
Gene co-expression module in CD8⁺ T cells
| Category | Inflammation |
|---|---|
| Genes | 10 |
| Annotation certainty | 4 of 5 |
| Annotation consistency | 9 of 10 genes have a known function matching the annotation |
Why this annotation
The hub genes and module members are strongly enriched for interferon-stimulated genes and antiviral response components. BST2 (tetherin), PLSCR1, EIF2AK2 (PKR), OASL, TAP1, NMI, and LAP3 are all classical ISGs or interferon-pathway effectors. BST2 restricts viral budding, EIF2AK2/PKR mediates antiviral translation inhibition, OASL is an OAS-like antiviral factor, TAP1 is involved in antigen presentation downstream of IFN-γ, and NMI (N-myc interactor) amplifies JAK-STAT signaling. CHMP5 (ESCRT-III) and NAPA are membrane trafficking components, likely co-regulated as part of the antiviral membrane remodeling response. SPATS2L is a lesser-characterized ISG. This module is a Type I/II interferon response module, neighboring the canonical ISG modules M0 and M69, consistent with a broader interferon neighborhood. It is slightly broader/less canonical than M0 (which contains the most archetypal IFN-α ISGs) and may capture IFN-γ-enriched or secondary-wave ISG programs.
Genes
BST2, CHMP5, EIF2AK2, LAP3, NAPA, NMI, OASL, PLSCR1, SPATS2L, TAP1
Most correlated modules
- Type I Interferon · correlation 0.88
- IFN-gamma Response · correlation 0.86
- Stress-ISG Response · correlation 0.83
- Interferon-stimulated Genes · correlation 0.80
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.