Complement-secreting Fibroblast
Gene co-expression module in Fibroblasts
| Category | Immune interaction |
|---|---|
| Genes | 18 |
| Annotation certainty | 3 of 5 |
| Annotation consistency | 10 of 18 genes have a known function matching the annotation |
Why this annotation
Hub genes include NPC2 (cholesterol transport/lysosomal), SERPING1 (complement C1 inhibitor), C1R (complement serine protease), C2 (complement component), IFITM2/IFITM3 (interferon-induced transmembrane proteins), GPX4 (glutathione peroxidase, lipid peroxide defense), FTH1/FTL (ferritin heavy/light chains, iron storage), FCGRT (neonatal Fc receptor), and VIM (vimentin, fibroblast marker). The complement components (SERPING1, C1R, C2) and interferon-stimulated genes (IFITM2, IFITM3) dominate the top-ranked genes. The module is downregulated in remission (both UC and CD) and slightly upregulated in CD inflammation, consistent with a baseline innate immune/complement-active fibroblast state. SERPING1 and C1R are classical markers of complement-producing stromal fibroblasts in the intestine. The co-expression of IFITM2/3 with complement genes suggests an interferon-primed, complement-secreting fibroblast program. Neighbor context: this module sits near housekeeping/translation modules (M67, M121, M29, M8, M69), suggesting it represents a constitutively expressed but biologically specific program in fibroblasts rather than a stress artifact.
Genes
ADI1, ARL6IP5, C1R, C2, CYB5A, FCGRT, FTH1, FTL, GPX4, GYPC, IFITM2, IFITM3, NPC2, OLFML3, PSIP1, RAB13, SERPING1, VIM
Most correlated modules
- Proteolytic Fibroblast State · correlation 0.89
- Translation Initiation · correlation 0.82
- Stromal Fibroblast Activation · correlation 0.81
- Homeostatic Fibroblast Identity · correlation 0.79
- ECM Homeostasis · correlation 0.77
- Microfibril ECM Fibroblast · correlation 0.76
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.