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TET2 guards against unchecked BATF3-induced CAR T cell expansion [RNA-seq]

ABSTRACT: Comparing transcriptional profiles of TET2 deficent hyper-proliferative CAR T cells and unedited CAR T cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE220258 | GEO | 2022/12/30

REPOSITORIES: GEO

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TET2 guards against unchecked BATF3-induced CAR T cell expansion [ATAC-seq]

Project description:Comparing genome accessibility profiles (ATACseq) of TET2 deficent hyper-proliferative CAR T cells and unedited CAR T cells

2022-12-30 | GSE220257 | GEO

TET2 guards against unchecked BATF3-induced CAR T cell expansion.

Project description:Further advances in cell engineering are needed to increase the efficacy of chimeric antigen receptor (CAR) and other T cell-based therapies1-5. As T cell differentiation and functional states are associated with distinct epigenetic profiles6,7, we hypothesized that epigenetic programming may provide a means to improve CAR T cell performance. Targeting the gene that encodes the epigenetic regulator ten-eleven translocation 2 (TET2)8 presents an interesting opportunity as its loss may enhance T cell memory9,10, albeit not cause malignancy9,11,12. Here we show that disruption of TET2 enhances T cell-mediated tumour rejection in leukaemia and prostate cancer models. However, loss of TET2 also enables antigen-independent CAR T cell clonal expansions that may eventually result in prominent systemic tissue infiltration. These clonal proliferations require biallelic TET2 disruption and sustained expression of the AP-1 factor BATF3 to drive a MYC-dependent proliferative program. This proliferative state is associated with reduced effector function that differs from both canonical T cell memory13,14 and exhaustion15,16 states, and is prone to the acquisition of secondary somatic mutations, establishing TET2 as a guardian against BATF3-induced CAR T cell proliferation and ensuing genomic instability. Our findings illustrate the potential of epigenetic programming to enhance T cell immunity but highlight the risk of unleashing unchecked proliferative responses.

| S-EPMC10511001 | biostudies-literature

TET2 guards against unchecked BATF3-induced CAR T cell expansion

Project description:TET2 guards against unchecked BATF3-induced CAR T cell expansion

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TET2 guards against unchecked BATF3-induced CAR T cell expansion [ATAC-seq]

Project description:TET2 guards against unchecked BATF3-induced CAR T cell expansion [ATAC-seq]

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TET2 guards against unchecked BATF3-induced CAR T cell expansion [RNA-seq]

Project description:TET2 guards against unchecked BATF3-induced CAR T cell expansion [RNA-seq]

| PRJNA909310 | ENA

TET2 guards against unchecked BATF3-induced CAR T cell expansion

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-12-30 | GSE220259 | GEO

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Project description:Drosophila melanogaster car, carnation, is differentially expressed in 11 experiment(s);

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The TET2 methylcytosine dioxygenase regulates early and late transitions in exhausted CD8+ T-cell differentiation

Project description:Epigenetic reprogramming of CAR T-cells by targeting TET2, a methylcytosine deoxygenase that mediates active DNA demethylation, has shown therapeutic potential; however, the role of TET2 in TEX development is unclear. In both CAR T-cell exhaustion models in vitro and chronic LCMV infection in vivo, TET2 drove the conversion from memory-like, self-renewing TEX progenitors towards effector (TEFF)-like and terminally differentiated TEX. TET2-deficient terminally differentiated TEX retained aspects of TEX progenitor biology, including decreased expression of the transcription factor TOX, suggesting that TET2 is required for terminal exhaustion.

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Expression data from chimeric antigen receptor transduced (CAR) human CD4+ T cells during expansion

Project description:In this data set we include expression data from human CD4+ T cells isolated on day 0, 6, 11 and 24 follow anti-CD3/anti-CD28 magnetic bead stimulation and chimeric antigen receptor transduction. 30 samples were submitted. Samples represented three biological replicates of normal donors transduced with various CARs. CARs used were a cMet 28z specific CAR comprised of the IgG4 hinge, CD28 transmembrane and CD28 and CD3zeta intracellular domains. A CD19 CD28 CAR was specific to CD19, and was comprised of a CD8a hinge, CD28 transmembrane and CD28 and CD3zeta intracellular domain. A third CAR, the CD19 BBz, was used that was specific to CD19 was comprised of a CD8a hinge, CD8a transmembrane and 4-1BB and CD3zeta intracellular domains. Expression data was analyzied on day 0, 6, 11 and 24.

2015-01-14 | E-GEOD-64914 | biostudies-arrayexpress

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