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Restricting tumor lactic acid metabolism using dichloroacetate improves T cell functions.
Hosein Rostamian1, Mohammad Khakpoor-Koosheh1, Leila Jafarzadeh1,2
1Department of Medical Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
BMC Cancer
|January 7, 2022
Summary
Tumor-produced lactic acid suppresses T cell function and immune response. Dichloroacetate (DCA) reduces tumor lactic acid, enhancing T cell proliferation, cytokine production, and anti-tumor activity.
Area of Science:
- Immunology
- Cancer Metabolism
Background:
- Tumor-derived lactic acid impairs T cell activation and function within the tumor microenvironment.
- Targeting tumor cell glycolysis may enhance immunosurveillance and tumor growth control.
Purpose of the Study:
- To investigate the impact of lactic acid on T cell activation, function, and redox state.
- To evaluate the effects of Dichloroacetate (DCA) on T cells in the context of reduced tumor lactic acid.
Main Methods:
- Assessed T cell proliferation, cytokine production, and redox balance (ROS, superoxide, glutathione).
- Analyzed gene expression related to the T cell redox system.
- Co-cultured T cells with DCA-treated tumor cells.
Main Results:
- Lactic acid suppressed T cell proliferation, cytokine production, and redox system function.
- DCA treatment reduced tumor lactic acid levels, boosting T cell proliferation and cytokine secretion.
- DCA rescued T cells from apoptosis.
Conclusions:
- Tumor lactic acid accumulation hinders T cell responses, potentially limiting T cell therapy efficacy.
- Dichloroacetate (DCA) promotes anti-tumor T cell responses via metabolic reprogramming of tumor cells.
