%0 Journal Article
%A Kaeuferle, Theresa
%A Zwermann, Maximilian
%A Stoll, Nadine
%A Ferrada-Ernst, Paulina
%A Jablonowski, Lena
%A Zeidler, Reinhard
%A Willier, Semjon
%A Stenger, Dana
%A Yassin, Abdallah
%A Stripecke, Renata
%A Feuchtinger, Tobias
%T All-in-one CRISPR/Cas-engineered glucocorticoid-receptor knock-out EBV-gp350-CAR knock-in T cells are potent and resistant to dexamethasone.
%J Experimental hematology & oncology
%V 14
%N 1
%@ 2162-3619
%C London
%I Biomed Central
%M DKFZ-2025-00663
%P 40
%D 2025
%X Epstein-Barr virus (EBV) reactivation in immunocompromised patients and post-transplantation is associated with morbidity, mortality and with the onset of a variety of malignant diseases. Adoptive T-cell therapies have emerged as promising therapeutic options, but post-transplant immunosuppression jeopardizes the protective anti-EBV immune surveillance by adoptively transferred T cells.Using an all-in-one CRISPR/Cas-mediated approach, we inserted an anti-EBV (gp350) CAR into the T-cell receptor (TRAC) locus and simultaneously knocked-out the glucocorticoid receptor (GR) on a good manufacturing practice (GMP)-compatible platform.CAR knock-in (CARKI) was confirmed in primary human T cells on genetic and on protein level with a mean efficiency of 41
%K Adoptive T cell transfer (Other)
%K CAR T cells (Other)
%K CRISPR/Cas (Other)
%K Dexamethasone (Other)
%K EBV (Other)
%K Genetic engineering (Other)
%K Glucocorticoid receptor (Other)
%K Steroid treatment (Other)
%F PUB:(DE-HGF)16
%9 Journal Article
%$ pmid:40108708
%2 pmc:PMC11921674
%R 10.1186/s40164-025-00631-w
%U https://inrepo02.dkfz.de/record/300186