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Nr2f6-deficient chimeric antigen receptor T cells
- Development stage
- Preclinical
- Lead developer
- Medical University of Innsbruck
- Modality
- CRISPR-Cas9 → CRISPR Systems → Programmable Nucleases → Gene Editing → Gene Therapies, CAR-T Cells → Engineered T Cells → Adoptive Cell Transfer → Cell Therapies
- Administration
- Intravenous
01
Overview
Nr2f6-deficient chimeric antigen receptor T cells are an experimental cell therapy engineered using gene editing to delete the NR2F6 gene, which encodes an intracellular immune checkpoint. NR2F6 normally functions as a negative regulator of T cell activation; its absence in CAR-T cells prevents exhaustion, maintains a progenitor-like state (TCF1+), and enhances metabolic fitness. This modification allows the cells to sustain cytotoxic activity in the immunosuppressive tumor microenvironment of solid tumors. Furthermore, these cells induce 'epitope spreading,' a process where the initial CAR-T activity triggers a broader, polyclonal host immune response against various tumor antigens, providing long-term protection even after the engineered cells are cleared. Preclinical studies have demonstrated efficacy in models of glioblastoma and pancreatic adenocarcinoma.
- Other names
- NR2F6-deleted CAR-T cellsNR-2F6-deleted CAR-T cellsNR 2F6-deleted CAR-T cellsNR2F6-knockout CAR-T cellsNR-2F6-knockout CAR-T cellsNR 2F6-knockout CAR-T cellsNr2f6-deficient CAR-T cellsNr-2f6-deficient CAR-T cellsNr 2f6-deficient CAR-T cells
02
Targets
NR2F6 (Nuclear receptor subfamily 2 group F member 6)
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