Summary of Study ST003167
This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001970. The data can be accessed directly via it's Project DOI: 10.21228/M8314P This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.
| Study ID | ST003167 |
| Study Title | Metabolomics of Human CD19-BBz CD8 CAR-T cells with low and high MCJ expression |
| Study Summary | The goal of these experiments are to characterize the metabolic profile of the human CD8 CD19-BBz CAR-T cells from donors with high or low MCJ expression after 3 expansions (6 days) with IL-2 (100IU/ml). |
| Institute | University of Colorado School of Medicine |
| Laboratory | Laboratory of Angelo D'Alessandro in collaboration with Mercedes Rincon |
| Last Name | Cendali |
| First Name | Francesca |
| Address | 13199 East Montview Boulevard, Aurora, CO, 80045, USA |
| francesca.cendali@cuanschutz.edu | |
| Phone | 3037246131 |
| Submit Date | 2024-04-11 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | raw(Thermo) |
| Analysis Type Detail | LC-MS |
| Release Date | 2024-05-02 |
| Release Version | 1 |
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Project:
| Project ID: | PR001970 |
| Project DOI: | doi: 10.21228/M8314P |
| Project Title: | Releasing the mitochondrial respiration brake MCJ/DnaJC15 enhances CD8 CAR-T cell therapy efficacy |
| Project Summary: | Metabolism of chimeric antigen receptor (CAR) T cells is emerging as an important area to improve CAR-T cell therapy in cancer treatment. Mitochondrial respiration is essential for survival and function of CAR-T cells, but developing strategies to specifically enhance mitochondrial respiration has been challenging. Here we identify MCJ/DnaJC15, an endogenous negative regulator of mitochondrial Complex I, as a metabolic target to enhance mitochondrial respiration in CD8 CAR-T cells. Loss of MCJ in CD8 CAR-T cells increases their in vitro and in vivo efficacy against mouse B cell leukemias. MCJ deficiency in TCR- specific CD8 cells also increases their efficacy against solid tumors in vivo. Furthermore, we reveal that human CD8 cells express MCJ and that silencing MCJ expression increases mitochondrial metabolism and anti-tumor activity of human CAR-T cells. Thus, targeting MCJ to enhance mitochondrial metabolism is a promising therapeutic strategy to improve the efficacy of adoptive T cell therapies. |
| Institute: | University of Colorado School of Medicine |
| Laboratory: | Laboratory of Angelo D'Alessandro in collaboration with Mercedes Rincon |
| Last Name: | Cendali |
| First Name: | Francesca |
| Address: | 13199 East Montview Boulevard, Aurora, CO, 80045, USA |
| Email: | francesca.cendali@cuanschutz.edu |
| Phone: | 3037246131 |
