CASTOR1 regulates humoral immune responses and contributes to the pathogenesis of systemic lupus erythematosus
What this study shows
Gives the arginine sensor CASTOR1 a defined physiological job upstream of mTORC1: losing it de-represses mTORC1 in B cells and drives plasma-cell expansion, IgG and anti-dsDNA autoantibodies, and lupus-like glomerulonephritis. In human SLE, CASTOR1 expression in plasmablasts was inversely correlated with disease activity (r = -0.32, p = 0.00031). One of the few studies to tie a specific upstream amino-acid sensor to a human autoimmune phenotype rather than to cancer or growth.
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Human B cells (ImmuNexUT transcriptomes, n=136 SLE patients) + whole-body and B cell-specific Castor1-knockout mice) rather than a whole-organism health-outcome study. That is often exactly where causal biology gets established -- the code says which system the finding was shown in, and nothing about how good the work is. |
| Study type | 5 - Mechanistic / In Vitro |
| Model system | Human B cells (ImmuNexUT transcriptomes, n=136 SLE patients) + whole-body and B cell-specific Castor1-knockout mice |
| Journal | Arthritis & Rheumatology |
| Year | 2026 |
| Peer reviewed | Yes |
| Record last updated | 2026-08-22 |
| Source | DOI 10.1002/art.70314 · PMID 42695806 |