Immature DC Metabolism
Gene co-expression module in Dendritic cells
| Category | Development |
|---|---|
| Genes | 0 |
| Annotation certainty | 3 of 5 |
| Annotation consistency | 10 of 25 genes have a known function matching the annotation |
Why this annotation
This module has very low expression and detection (mean 0.143, 13.9% positive) with 'not detected' as top subset, yet most genes show extreme mDC enrichment when expressed. Key genes: LAD1 (184x mDC — a keratin-associated protein, potentially contamination marker but also expressed in some epithelial-like states), TMEM176A/B (immature DC markers, negative regulators of DC activation), AOC1 (amine oxidase, highly mDC-enriched), NMRK1 (NAD biosynthesis), H6PD (hexose-6-phosphate dehydrogenase, ER redox), ARHGAP10 (Rho GAP), SLCO5A1 (solute carrier), IL32 (pro-inflammatory cytokine), CYB5A (cytochrome b5, ER redox/lipid metabolism), KIF2A (kinesin, microtubule dynamics), TUBB6 (tubulin), NDE1 (nuclear distribution element, microtubule), GRSF1 (mitochondrial RNA binding). The combination of TMEM176A/B (immature DC markers), metabolic genes (H6PD, NMRK1, CYB5A), and cytoskeletal genes (KIF2A, TUBB6, NDE1) in a low-expression, inflammation-upregulated module suggests an immature/transitional mDC metabolic state. TMEM176A and TMEM176B are canonical markers of immature/tolerogenic DCs that are downregulated upon activation — their presence here alongside inflammation upregulation may reflect a transitional population. The module is best characterized as an immature DC metabolic program.
Genes
Most correlated modules
- mDC Inflammatory Activation · correlation 0.96
- mTOR Nutrient Sensing · correlation 0.95
- Tolerogenic mDC · correlation 0.94
- Death Receptor Signaling · correlation 0.91
- DC Maturation Migration · correlation 0.87
- Epigenetic Regulation · correlation 0.87
- Lysosomal Trafficking Regulation · correlation 0.86
- Chromatin Remodeling · correlation 0.83
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.