TCR Signal Attenuation
Gene co-expression module in Mucosal-associated invariant T cell
| Category | Immune regulation |
|---|---|
| Genes | 17 |
| Annotation certainty | 3 of 5 |
| Annotation consistency | 8 of 17 genes have a known function matching the annotation |
Why this annotation
This module contains several functionally coherent immune-regulatory genes. DUSP16 is a MAP kinase phosphatase that negatively regulates JNK/MAPK signaling downstream of TCR. PTPN22 is a key negative regulator of T cell activation (tyrosine phosphatase). PPP2R5C is a PP2A regulatory subunit involved in dephosphorylation of signaling molecules. LAX1 (linker for activation of X cells) is an adaptor that negatively regulates lymphocyte activation. FAS (CD95) mediates apoptosis in activated T cells. CRACR2A regulates store-operated calcium entry and TCR-proximal signaling. CHD2 is a chromatin remodeler involved in immune gene regulation. AFF4 is part of the super elongation complex regulating transcription. YTHDC1 is an m6A RNA reader with roles in RNA processing. TRA2A regulates splicing. FNBP1 links membrane dynamics to actin. MVB12B is part of ESCRT-I. CENPC, OFD1, BORCS5 are involved in centrosome/lysosome biology. The dominant theme is negative regulation of TCR/lymphocyte signaling (DUSP16, PTPN22, PPP2R5C, LAX1, FAS, CRACR2A), consistent with immune checkpoint/regulation in MAIT cells.
Genes
AFF4, BORCS5, CENPC, CHD2, CRACR2A, CRYBG1, DUSP16, FAS, FNBP1, LAX1, MVB12B, OFD1, PNN, PPP2R5C, PTPN22, TRA2A, YTHDC1
Most correlated modules
- Hypoxia-ER Stress · correlation 0.89
- Nuclear-Cytoplasmic Transport · correlation 0.81
- T cell Quiescence · correlation 0.79
- MAIT Cell Identity · correlation 0.78
- Post-translational Regulation · correlation 0.77
- Circadian Transcriptional Regulation · correlation 0.76
- Cytoskeletal Organization · correlation 0.73
- Nuclear Receptor Chromatin · correlation 0.72
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.