NF-κB/IFN Inflammatory
Gene co-expression module in Glial cells
| Category | Inflammation |
|---|---|
| Genes | 13 |
| Annotation certainty | 5 of 5 |
| Annotation consistency | 11 of 13 genes have a known function matching the annotation |
Why this annotation
This module is strongly upregulated in both UC and CD inflammation (delta_inflammation scores ~1.7-1.8, significant) and returns toward baseline with remission, indicating a disease-active inflammatory program. Hub genes include SOD2 (oxidative stress response, NF-κB target), ICAM1 (adhesion molecule, hallmark of inflammatory activation), UBD (ubiquitin-like modifier, ISG/NF-κB target), CXCL2, CXCL9, CXCL10 (inflammatory chemokines — CXCL9/10 are IFN-γ-induced, CXCL2 is NF-κB-driven), CTSS (cathepsin S, immune activation marker), PTX3 (acute phase/innate immunity), BIRC3 (NF-κB target, anti-apoptotic), TRIB1 (NF-κB/MAPK signaling), and WTAP (m6A methyltransferase, inflammation-linked). HAPLN3 and FDCSP are less canonical but present in inflammatory microenvironments. The module is coherent (core), uniformly distributed across glial subsets, and its entire signature is consistent with NF-κB/IFN-γ-driven inflammatory activation in glial cells during IBD. The co-expression of IFN-γ-response chemokines (CXCL9, CXCL10) with NF-κB targets (ICAM1, BIRC3, SOD2, CXCL2) is characteristic of a combined innate/adaptive inflammatory response. No technical artifact or contamination signals are present.
Genes
BIRC3, CTSS, CXCL10, CXCL2, CXCL9, FDCSP, HAPLN3, ICAM1, PTX3, SOD2, TRIB1, UBD, WTAP
Most correlated modules
- IFN-gamma Effector Program · correlation 0.86
- Inflammatory Cytokine Signaling · correlation 0.84
- Type I/II Interferon Response · correlation 0.73
- MHC-II Antigen Presentation · correlation 0.57
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.