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CRISPR/Cas9 mediated deletion of the adenosine A2AR enhances CAR T cell efficacy

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE156192 | GEO | 2021/03/29

REPOSITORIES: GEO

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CRISPR/Cas9 mediated deletion of the adenosine A2AR enhances CAR T cell efficacy [murine_CRISPR_A2AKO_RNA-seq]

Project description:Investigation of the transcriptional profile of stimulated murine CRISPR/Cas9 MOCK and A2ARKO α-HER2 CAR T cells in the presence/absence of NECA

2021-03-29 | GSE156191 | GEO

CRISPR/Cas9 mediated deletion of the adenosine A2AR enhances CAR T cell efficacy [human_CRISPR_A2AKO_RNA-seq]

Project description:Investigation of the transcriptional profile of stimulated HUMAN CRISPR/Cas9 MOCK and A2ARKO α-lewisY CAR T cells in the presence/absence of NECA

2021-03-29 | GSE156190 | GEO

CRISPR/Cas9 mediated deletion of the adenosine A2AR enhances CAR T cell efficacy [NECA_RNA-seq]

Project description:Investigation of the transcriptional profile of stimulated murine α-HER2 CAR T cells in the presence/absence of NECA and/or SCH58261

2021-03-29 | GSE156189 | GEO

CRISPR/Cas9 mediated deletion of the adenosine A2A receptor enhances CAR T cell efficacy.

Project description:Adenosine is an immunosuppressive factor that limits anti-tumor immunity through the suppression of multiple immune subsets including T cells via activation of the adenosine A2A receptor (A2AR). Using both murine and human chimeric antigen receptor (CAR) T cells, here we show that targeting A2AR with a clinically relevant CRISPR/Cas9 strategy significantly enhances their in vivo efficacy, leading to improved survival of mice. Effects evoked by CRISPR/Cas9 mediated gene deletion of A2AR are superior to shRNA mediated knockdown or pharmacological blockade of A2AR. Mechanistically, human A2AR-edited CAR T cells are significantly resistant to adenosine-mediated transcriptional changes, resulting in enhanced production of cytokines including IFNγ and TNF, and increased expression of JAK-STAT signaling pathway associated genes. A2AR deficient CAR T cells are well tolerated and do not induce overt pathologies in mice, supporting the use of CRISPR/Cas9 to target A2AR for the improvement of CAR T cell function in the clinic.

| S-EPMC8163771 | biostudies-literature

CRISPR/Cas9 mediated deletion of the adenosine A2AR enhances CAR T cell efficacy

Project description:CRISPR/Cas9 mediated deletion of the adenosine A2AR enhances CAR T cell efficacy

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CRISPR/Cas9 mediated deletion of the adenosine A2AR enhances CAR T cell efficacy [NECA_RNA-seq]

Project description:CRISPR/Cas9 mediated deletion of the adenosine A2AR enhances CAR T cell efficacy [NECA_RNA-seq]

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CRISPR/Cas9 mediated deletion of the adenosine A2AR enhances CAR T cell efficacy [human_CRISPR_A2AKO_RNA-seq]

Project description:CRISPR/Cas9 mediated deletion of the adenosine A2AR enhances CAR T cell efficacy [human_CRISPR_A2AKO_RNA-seq]

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CRISPR/Cas9 mediated deletion of the adenosine A2AR enhances CAR T cell efficacy [murine_CRISPR_A2AKO_RNA-seq]

Project description:CRISPR/Cas9 mediated deletion of the adenosine A2AR enhances CAR T cell efficacy [murine_CRISPR_A2AKO_RNA-seq]

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Adenosine A2A receptor (A2AR) stimulation enhances mitochondrial metabolism and mitigates reactive oxygen species-mediated mitochondrial injury.

Project description:In OA chondrocytes, there is diminished mitochondrial production of ATP and diminished extracellular adenosine resulting in diminished adenosine A2A receptor (A2AR) stimulation and altered chondrocyte homeostasis which contributes to the pathogenesis of OA. We tested the hypothesis that A2AR stimulation maintains or enhances mitochondrial function in chondrocytes. The effect of A2AR signaling on mitochondrial health and function was determined in primary murine chondrocytes, a human chondrocytic cell line (T/C-28a2), primary human chondrocytes, and a murine model of OA by transmission electron microscopy analysis, mitochondrial stress testing, confocal live imaging for mitochondrial inner membrane polarity, and immunohistochemistry. In primary murine chondrocytes from A2AR-/- null mice, which develop spontaneous OA by 16 weeks, there is mitochondrial swelling, dysfunction, and reduced mitochondrial content with increased reactive oxygen species (ROS) burden and diminished mitophagy, as compared to chondrocytes from WT animals. IL-1-stimulated T/C-28a2 cells treated with an A2AR agonist had reduced ROS burden with increased mitochondrial dynamic stability and function, findings which were recapitulated in primary human chondrocytes. In an obesity-induced OA mouse model, there was a marked increase in mitochondrial oxidized material which was markedly improved after intraarticular injections of liposomal A2AR agonist. These results are consistent with the hypothesis that A2AR ligation is mitoprotective in OA.

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A Highly Efficient CRISPR-Cas9-Mediated Large Genomic Deletion in Bacillus subtilis.

Project description:In Bacillus subtilis, large genomic deletions have been carried out for genome reduction, antibiotic overproduction, and heterologous protein overexpression. In view of the eco-friendliness of B. subtilis, it is critical that engineering preserves its food-grade status and avoids leaving foreign DNA in the genome. Existing methods of generating large genomic deletions leave antibiotic resistance markers or display low mutation efficiency. In this study, we introduced a clustered regularly interspaced short palindromic repeat-derived genome engineering technique to develop a highly efficient method of generating large genomic deletions in B. subtilis without any trace of foreign DNA. Using our system, we produced 38 kb plipastatin-synthesizing pps operon deletion with 80% efficiency. The significant increase in mutation efficiency was due to plasmids-delivered Streptococcus pyogenes-originated SpCas9, target-specific sgRNA and a donor DNA template, which produces SpCas9/sgRNA endonuclease complex continuously for attacking target chromosome until the mutagenic repair occurs. Our system produced single-gene deletion in spo0A (∼100%), point mutation (∼68%) and GFP gene insertion (∼97%) in sigE and demonstrated its broad applicability for various types of site-directed mutagenesis in B. subtilis.

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