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Electroporation of Functional Bacterial Effectors into Mammalian Cells

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Acetate Promotes T Cell Effector Function during Glucose Restriction.

Jing Qiu¹, Matteo Villa¹, David E Sanin¹

¹Max Planck Institute of Immunobiology and Epigenetics, Freiburg 79108, Germany.

|May 16, 2019

Summary

This summary is machine-generated.

Acetate can restore function in glucose-deprived CD8+ T cells by enhancing epigenetic modifications and cytokine production. This suggests targeting alternative nutrient utilization pathways may improve anti-cancer T cell responses.

Keywords:

T cell exhaustion T cell hyporesponsiveness T cells acetate acetyl-CoA synthetase chromatin remodeling effector functions tumor immunity tumor-infiltrating lymphocytes

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Area of Science:

Immunology
Metabolic pathways in cancer
Epigenetics

Background:

Nutrient competition, particularly for glucose, impairs T cell function in the tumor microenvironment.
Cancer cells utilize alternative substrates like acetate for their metabolism and growth.

Purpose of the Study:

To investigate the role of acetate in rescuing effector function of glucose-restricted CD8+ T cells.
To elucidate the mechanisms by which acetate impacts T cell metabolism and function in cancer.

Main Methods:

Assessing effector function of CD8+ T cells in glucose-limited conditions with and without acetate.
Analyzing histone acetylation, chromatin accessibility, and IFN-γ gene transcription.
Evaluating the impact of acetyl-CoA synthetase (ACSS) expression on T cell function and tumor clearance.

Main Results:

Acetate rescues effector function in glucose-restricted CD8+ T cells.
Acetate enhances histone acetylation, chromatin accessibility, and IFN-γ production via ACSS.
Ex vivo acetate treatment boosts IFN-γ in exhausted T cells; reduced ACSS impairs T cell function and tumor clearance.

Conclusions:

Acetate can epigenetically remodel and reactivate hyporesponsive T cells in a glucose-deficient tumor microenvironment.
Targeting metabolic pathways that utilize alternative substrates like acetate presents a potential therapeutic strategy to enhance anti-cancer T cell immunity.