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Allogeneic HSPC-engineered CD33-targeting CAR-NKT cells synergize with hypomethylating agents for effective and safe treatment of myeloid malignancies

ABSTRACT: Allogeneic HSPC-engineered CD33-targeting CAR-NKT cells synergize with hypomethylating agents for effective and safe treatment of myeloid malignancies

PROVIDER: PRJNA1126626 | ENA |

REPOSITORIES: ENA

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Allogeneic HSPC-engineered CD33-targeting CAR-NKT cells synergize with hypomethylating agents for effective and safe treatment of myeloid malignancies

Project description:Chimeric antigen receptor (CAR)-engineered T cell therapy holds promise for targeting myeloid malignancies including acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS). However, autologous approaches pose significant challenges in manufacturing and patient selection, emphasizing the need for off-the-shelf cell products. In this study, we systematically characterized primary AML and MDS patient samples, identifying a unique therapeutic opportunity for CAR-engineered invariant natural killer T (CAR-NKT) cell therapy. Utilizing a clinically guided culture method, we generated allogeneic IL-15-enhanced CD33-targeting CAR-NKT (Allo15CAR33-NKT) cells through HSPC engineering and an ex vivo, feeder-free HSPC differentiation culture. These cells demonstrated potent antitumor efficacy against blast cells via multiple tumor-targeting mechanisms. In vivo, Allo15CAR33-NKT cells exhibited effective tumor homing, expansion, and persistence, characterized by high effector function and low exhaustion propensity. Furthermore, these cells synergized with hypomethylating agent (HMA) treatment, which upregulated CD1d and NK ligand expression on tumor cells, enhancing susceptibility to Allo15CAR33-NKT cell-mediated killing. Notably, Allo15CAR33-NKT cells displayed minimal off-tumor effects against hematopoietic precursors, and low risks of graft-versus-host disease and cytokine release syndrome, highlighting their substantial therapeutic potential for myeloid malignancies.

2025-01-01 | GSE270430 | GEO

RNA expression profiling of CD13/CD33-positive and CD13/CD33-negative B-ALL patients [miRNA expression]

Project description:To study the effect of expression of CD13/CD33 on the pathogenesis of B-cell acute lymphoblastic (B-ALL), we collected samples from 4 CD13/CD33-positive and 4 CD13/CD33-negative B-ALL patients and performed RNA-seq.

2023-12-31 | GSE197180 | GEO

RNA expression profiling of CD13/CD33-positive and CD13/CD33-negative B-ALL patients [mRNA expression]

2023-12-31 | GSE197178 | GEO

Genome-wide expression profile on hiPSCs and hiPSC-derived CD33+ myeloid cells

Project description:To gain insights into which pathways might be dysregulated in JMML, we compared the transcriptome profiles among hiPSC and sorted CD33+ myeloid cells from control and patient samples. NS/JMML-derived CD33+ myeloid cells showed dysregulation in major biological processes. Moreover, a consistent expression pattern among sets of genes related to pluripotency and myeloid regulation was observed in the control, NS and NS/JMML CD33+ myeloid cells further supporting generally successful myelopoiesis. Total RNA obtained from hiPSC and sorted CD33+ myeloid cells (at day 14 of differentiation) from control and patient samples

2014-01-31 | E-GEOD-54538 | biostudies-arrayexpress

RNA-seq of CD33 KO and control HSPCs

Project description:Gene expression profile of in vitro differentiated control and CD33 KO CD34+ cells (with 70-85% CD33 KO) were analyzed by RNA-seq to exclude any major impact of CD33 loss on downstream gene expression

2018-04-26 | GSE113670 | GEO

HSPC scRNA seq

Project description:HSPC scRNA seq

| PRJNA627730 | ENA

TREM2 Acts Downstream of CD33 in Modulating Microglial Pathology in Alzheimer's Disease

Project description:CD33-/- and/or TREM2-/- mice were crossed with the 5xFAD mouse model of Alzheimer’s disease to generate single and double CD33/TREM2 knock-out mice on 5xFAD background. Transcriptome and gene expression analyses were performed to analyze the impact of CD33 and/or TREM2 knock-out on the transcriptome of microglia in the context of amyloid pathology. The results revealed that CD33 and/or TREM2 knock-out reprogrammed microglial gene expression signatures in 5xFAD mice in an age-dependent manner. Differential gene expression in 5xFAD;CD33-/- microglia depended on the presence of TREM2. These data suggest that TREM2 acts downstream of CD33.

2019-06-11 | GSE132508 | GEO

thermal proteome profiling of hypomethylating agents in infant ALL

Project description:thermal proteome profiling of hypomethylating agents in infant ALL for elucidation of their mode of action.

2022-11-15 | PXD030539 | Pride

Genome-wide expression profile on hiPSCs and hiPSC-derived CD33+ myeloid cells

2014-01-31 | GSE54538 | GEO

Deletion of the Alzheimer’s Disease-associated CD33 results in increased phagocytosis, oxidative burst and inflammation

Project description:In this study, wild type and CD33 knockout human THP1 macrophages were treated with control shRNA or shRNA against the CD33 signaling-associated protein tyrosine phosphatase PTPN6 and analyzed by mRNA sequencing. Whole genome transcriptome analysis showed that knockout of CD33 as well as knockdown of PTPN6 led to constitutive activation of inflammation-related pathways. On the other hand, PTPN6 knockdown was associated with changes in cell cycle and mitosis-related pathways in a CD33-deficient background.

2021-01-31 | GSE155567 | GEO

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