cAMP-Glucocorticoid Suppression
Gene co-expression module in Innate lymphoid cells
| Category | Immune regulation |
|---|---|
| Genes | 12 |
| Annotation certainty | 2 of 5 |
| Annotation consistency | 6 of 12 genes have a known function matching the annotation |
Why this annotation
PDE4D and PDE3B are phosphodiesterases that hydrolyze cAMP, a key second messenger suppressing NK/T cell activation. NR3C1 (glucocorticoid receptor) mediates immunosuppressive glucocorticoid signaling and is directly relevant to treatment response (delta_treatment_CD = -0.428, the strongest treatment signal in this batch). SH2D2A (TSAd) modulates TCR/NK signaling. NEK7 activates NLRP3 inflammasome. CERK (ceramide kinase) participates in lipid signaling. CD7 marks T/NK cells. The strong negative treatment response in CD and the PDE/NR3C1 axis suggest this module captures cAMP-mediated and glucocorticoid-mediated immune suppression, potentially reflecting a treatment-sensitive regulatory state. Weak coherence limits confidence.
Genes
CD7, CERK, CNDP2, COA1, NAP1L4, NEK7, NR3C1, PDE3B, PDE4D, RNASET2, SH2D2A, STAU1
Most correlated modules
- IFN-driven ILC1 Activation · correlation 0.91
- Lymphocyte Apoptosis Regulation · correlation 0.75
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.