NK Immune Checkpoint
Gene co-expression module in Natural Killer cells
| Category | Immune regulation |
|---|---|
| Genes | 10 |
| Annotation certainty | 3 of 5 |
| Annotation consistency | 7 of 10 genes have a known function matching the annotation |
Why this annotation
Hub genes include PTPN22 (protein tyrosine phosphatase non-receptor type 22, major negative regulator of TCR/BCR and NK cell signaling, IBD/autoimmunity risk gene), RANBP2 (RAN binding protein 2, nuclear pore complex, SUMOylation), SAMSN1 (SAM and SH3 domain-containing protein, negative regulator of B/NK cell activation), P2RY10 (purinergic receptor), STAT4 (transcription factor critical for NK cell IFN-γ production and IL-12 signaling), AKAP13 (A-kinase anchoring protein, RhoA GEF activity), G3BP2 (stress granule assembly, Ras-GAP binding), LIMS1 (LIM and senescent cell antigen-like domain, integrin signaling), CHD1 (chromatin remodeler), and MORF4L2 (chromatin/transcription regulation). The module is significantly upregulated in CD inflammation. PTPN22, SAMSN1, and STAT4 are canonical NK/lymphocyte activation regulators. STAT4 drives IFN-γ in NK cells downstream of IL-12/IL-18. PTPN22 is a well-known IBD susceptibility gene. This module represents NK cell immune checkpoint/activation regulation in CD inflammation.
Genes
AKAP13, CHD1, G3BP2, LIMS1, MORF4L2, P2RY10, PTPN22, RANBP2, SAMSN1, STAT4
Most correlated modules
- MAPK/AP-1 Signaling · correlation 0.82
- NK Cell Activation · correlation 0.81
- NRF2 Stress Response · correlation 0.81
- mRNA Splicing · correlation 0.77
- NK Inflammatory Activation · correlation 0.71
- TGF-β Antagonism · correlation 0.71
- Glucocorticoid Response · correlation 0.71
- Hypoxia Response · correlation 0.69
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.