CAR-T against stroma: fibroblasts and myeloid cells
Instead of attacking the cancer cell, engineering T cells to strip away the scaffolding and the suppressive immune cells that protect it.
FAP-directed CAR-T depletes cancer-associated fibroblasts and, in mouse models, opens desmoplastic tumours to chemotherapy and immunity; a small Swiss study delivered FAP CAR-T into the pleural cavity in mesothelioma. Myeloid-directed approaches target CSF1R, TREM2, or CD163 populations. The recurring problem is that FAP and myeloid markers are not tumour-specific: FAP is expressed in bone-marrow stroma and healing tissue, and murine FAP CAR-T caused cachexia and marrow toxicity in early studies.
How it works
A CAR recognises a stromal antigen rather than a tumour antigen; killing the supporting cells collapses the niche the tumour depends on.
- Stroma is genetically stable, so it cannot mutate away
- One construct could serve many cancers
- Combines with drugs that stroma currently blocks
- On-target off-tumour toxicity: marrow, wound healing, cachexia
- No registrational programme
- Depleting stroma accelerated disease in some pancreatic models
Latest papers
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