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Boosting metabolism in T cells: a tool to improve T cell therapy for chronic lymphocytic leukemia patients

Project description

Improving immunotherapy efficiency in chronic lymphocytic leukemia

Chimeric antigen receptor (CAR) T-cell cancer immunotherapy is a promising novel strategy that makes use of a patient's own immune cells. However, in contrast to the success of CAR T cells in aggressive leukemia, their effect in the B-cell malignancy chronic lymphocytic leukemia (CLL, the most common leukemia in the Western World) is limited. Preliminary work shows defects in CLL-derived T-cell metabolism as a plausible causative factor. The EU-funded BOOTCAMP project aims to define the molecular mechanisms of (metabolic) alterations in CLL-derived T cells and elucidate how CLL cells reprogram T-cell metabolism. The project will provide crucial insight into the interplay between CLL and T cells, and the underlying failure of cancer immune surveillance. This may lead to metabolism-based curative autologous T cell based therapies in CLL, which may also be relevant for other malignancies.

Objective

Chronic lymphocytic leukemia (CLL) is the most common leukemia in the Western world. Novel targeted drugs are effective, but not curative. Moreover, prolonged use is associated with development of resistance, toxicity, and high economic cost. Allogeneic stem cell transplantation, which evokes a T cell mediated response, is potentially curative yet is associated with high graft-vs-host-related mortality. Therefore, an autologous T cell-based approach, e.g. chimeric antigen receptor T cells (CAR-T), is a highly promising strategy. However, in contrast to the success of CAR-T cells in aggressive leukemia, their effect in CLL is limited owing to a largely unexplained acquired T cell dysfunction in this disease setting.

I recently found that CLL cells impose a reduction in mitochondrial fitness and altered glucose metabolism on T cells, which may underlie the acquired T cell dysfunction. Lending clinical significance to this finding, I observed that the success of CAR-T treatment in CLL patients is highly associated with their mitochondrial biogenic capacity. I therefore hypothesize that improving mitochondrial fitness of CAR-T cells may offer a path to cure CLL.

I aim to:
1. Characterize the molecular mechanisms of metabolic alterations in CLL-derived T cells
2. Elucidate how CLL cells reprogram T cells metabolism
3. Increase mitochondrial biogenesis and fitness in CAR-T cells to improve therapeutic efficacy

To achieve these goals, I will conduct an array of complementary molecular, metabolic, and genetic assays using patient samples and a murine model of CLL. To address therapeutic potential I will study murine and human CAR-T cells in which metabolic processes will be manipulated.

This project provides crucial insight into the interplay between CLL and T cells, and the underlying failure of cancer immune surveillance. This may lead to metabolism-based curative autologous T cell based therapies in CLL, which may also be relevant for other malignancies.

Fields of science (EuroSciVoc)

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Programme(s)

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Topic(s)

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Funding Scheme

Funding scheme (or “Type of Action”) inside a programme with common features. It specifies: the scope of what is funded; the reimbursement rate; specific evaluation criteria to qualify for funding; and the use of simplified forms of costs like lump sums.

ERC-COG - Consolidator Grant

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Call for proposal

Procedure for inviting applicants to submit project proposals, with the aim of receiving EU funding.

(opens in new window) ERC-2019-COG

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Host institution

STICHTING AMSTERDAM UMC
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 1 647 662,00
Total cost

The total costs incurred by this organisation to participate in the project, including direct and indirect costs. This amount is a subset of the overall project budget.

€ 1 647 662,00

Beneficiaries (3)

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