IL-18 Innate Activation
Gene co-expression module in Mucosal-associated invariant T cell
| Category | Inflammation |
|---|---|
| Genes | 12 |
| Annotation certainty | 3 of 5 |
| Annotation consistency | 6 of 12 genes have a known function matching the annotation |
Why this annotation
IL18RAP is the accessory chain of the IL-18 receptor and is a defining marker of MAIT cell innate-like activation — IL-18 together with IL-12 drives cytokine-mediated MAIT activation independently of TCR. MYBL1 (A-MYB) is expressed in innate-like lymphocytes and germinal center B cells and regulates proliferation. RUNX2 is a RUNX family transcription factor that in lymphocytes contributes to effector differentiation. ADAM10 is a metalloprotease that sheds surface ligands (including CD56/NCAM1 from neighbor M80) modulating immune cell interactions. P2RY14 is a purinergic receptor expressed on immune cells responding to extracellular nucleotides as danger signals. ME1 (malic enzyme) supports NADPH production and metabolic reprogramming in activated cells. PARP8 participates in DNA repair. NEO1 (neogenin) and RBMS1 are regulatory. The IL18RAP-centered innate cytokine responsiveness combined with MYBL1 and RUNX2 points to an innate-like MAIT activation module driven by cytokine (IL-18) rather than TCR signals. This neighbors M78/M9 which contain broader T cell regulatory programs, consistent with effector MAIT states.
Genes
ADAM10, COLQ, IL18RAP, KIF5C, ME1, MYBL1, NEO1, P2RY14, PARP8, RBMS1, RUNX2, ZNF831
Most correlated modules
- SWI/SNF Chromatin Remodeling · correlation 0.74
- Cytoskeletal Migration · correlation 0.72
- TCR Signal Attenuation · correlation 0.72
- TCR Activation Signaling · correlation 0.72
- Circadian Transcriptional Regulation · correlation 0.70
- Cellular Maintenance · correlation 0.68
- T cell Transcriptional Identity · correlation 0.66
- RAS-GEF Signaling · correlation 0.65
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.