Fc Receptor Phagocytosis
Gene co-expression module in Macrophages
| Category | Lysosomal & pahgocytosis |
|---|---|
| Genes | 19 |
| Annotation certainty | 3 of 5 |
| Annotation consistency | 13 of 19 genes have a known function matching the annotation |
Why this annotation
The top hub genes are canonical myeloid/macrophage innate immune receptors and phagocytic machinery. FCGR1A (CD64, high-affinity Fc-gamma receptor I), FCGR3A (CD16, Fc-gamma receptor III), LY96 (MD-2, TLR4 co-receptor for LPS sensing), TREM2 (triggering receptor on myeloid cells 2, phagocytosis/lipid sensing), CD37 (tetraspanin, myeloid signaling), MNDA (myeloid nuclear differentiation antigen), FPR1 (formyl peptide receptor, innate chemotaxis), PILRA (paired immunoglobulin-like receptor A, inhibitory myeloid receptor), SUCNR1 (succinate receptor, inflammatory macrophage activation), HTRA1 (serine protease, ECM remodeling/macrophage), PON2 (paraoxonase 2, oxidative stress/macrophage), ANXA6 (annexin A6, phagocytic membrane), TRAF3IP3 (TRAF3-interacting, innate signaling), TNFSF12 (TWEAK, myeloid cytokine). This module represents a classical innate immune receptor and phagocytic recognition program in monocytes/macrophages. All genes show weak membership and unknown coherence, but the functional convergence on Fc-receptor-mediated phagocytosis and innate pattern recognition is strong. The mono_mac enrichment for key genes (TREM2, FCGR3A, PILRA, FPR1) is consistent with tissue macrophage identity. This module neighbors M18 (hypoxia/stress), which shares the mono_mac context, suggesting these are co-expressed programs in the same cell state.
Genes
ANXA6, C1orf162, CD37, FCGR1A, FCGR3A, FPR1, GCA, HNMT, HTRA1, ITGA6, LY96, MNDA, PILRA, PON2, SCP2, SUCNR1, TNFSF12, TRAF3IP3, TREM2
Most correlated modules
- Monocyte Phagocytic Identity · correlation 0.95
- Oxidative Metabolic Program · correlation 0.93
- Myeloid Immune Checkpoint · correlation 0.88
- Hypoxia Stress Response · correlation 0.82
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.