ArticleMolecular and cellular biochemistry2026
EF-1α-driven nanobody-based CD19-redirected CAR-T cells retain the antitumor efficacy, antigen-driven expansion, and cytokine secretion of CMV-driven counterparts.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chimeric antigen receptor (CAR) T-cell efficacy requires sustained transgene expression. Cytomegalovirus (CMV) promoters drive strong initial expression but undergo silencing, while elongation factor-1α (EF-1α) promoters resist inactivation. This study evaluated whether transitioning a previously established VHH-based CD19-redirected CAR construct to EF-1α promoter control compromises antitumor functionality. Lentiviral particles encoding identical second-generation CAR constructs (CD19-specific VHH, CD8α transmembrane, 4-1BB costimulatory, CD3ζ signaling domains) under CMV (HCAR-T) or EF-1α (ECAR-T) promoters transduced primary human T cells. Cytotoxicity (effector-to-target ratios 1:1-10:1), antigen-driven proliferation, and cytokine secretion against CD19⁺/CD19⁻ targets were quantified. Promoter substitution from CMV to EF-1α in the matched VHH-based CAR construct did not alter CAR-T cell functionality. ECAR-T and HCAR-T cells exhibited statistically comparable cytotoxicity against CD19⁺ Raji (81.6% ± 2.4 versus 81.8% ± 2.5 at 10:1, respectively) and NALM6 cells (82.2% ± 2.3 versus 80.7% ± 3.5 at 10:1, respectively). Proliferation against Raji (ECAR-T: 94.2% ± 7.54 versus HCAR-T: 91.1% ± 6.03) and NALM6 (ECAR-T: 94.9% ± 4.35 versus HCAR-T: 92.5% ± 6.34) was comparable. IFN-γ, IL-2, and TNF-α secretion against CD19⁺ targets was statistically comparable between ECAR-T and HCAR-T groups and strictly CD19-dependent. EF-1α preserved the antitumor potency of nanobody-based CD19-redirected CAR-T cells, supporting its use as a clinically relevant promoter for further development of this VHH-based CAR-T cell platform.
Indexed as
Identifiers
42455247What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.