期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 216, 期 12, 页码 2869-2882出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20182044
关键词
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资金
- New Faculty Startup fund from UCLA
- National Institutes of Health [DP2 CA196335]
- UCLA Tumor Immunology Training Grant (US Department of Health and Human Services Ruth L. Kirschstein Institutional National Research Service Award) [T32 CA009056]
- UCLA Broad Stem Cell Center Predoctoral Fellowship
T cells demand massive energy to combat cancer; however, the metabolic regulators controlling antitumor T cell immunity have just begun to be unveiled. When studying nutrient usage of tumor-infiltrating immune cells in mice, we detected a sharp increase of the expression of a CrT (Slc6a8) gene, which encodes a surface transporter controlling the uptake of creatine into a cell. Using CrT knockout mice, we showed that creatine uptake deficiency severely impaired antitumor T cell immunity. Supplementing creatine to WT mice significantly suppressed tumor growth in multiple mouse tumor models, and the combination of creatine supplementation with a PD-1/PD-11 blockade treatment showed synergistic tumor suppression efficacy. We further demonstrated that creatine acts as a molecular battery conserving bioenergy to power T cell activities. Therefore, our results have identified creatine as an important metabolic regulator controlling antitumor T cell immunity, underscoring the potential of creatine supplementation to improve T cell-based cancer immunotherapies.
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