Journal
INTERNATIONAL JOURNAL OF CANCER
Volume 151, Issue 5, Pages 797-808Publisher
WILEY
DOI: 10.1002/ijc.34059
Keywords
CD8(+) T cells; immunometabolism; immunotherapy; memory T cells; TCR signaling
Categories
Funding
- CRI Lloyd J. Old STAR Award [3914]
- Deutsche Forschungsgemeinschaft [259332240/RTG2099, CU375/5-1, CU375/5-2, CU375/7-1, CU375/9-1]
- EMBO Young Investigator Award
- ERC Consolidator Award [101045416]
- Helmholtz Young Investigator Award [VH-NG-1113]
- HI-TRON Kick-Start Seed Funding [HITR-2021-08]
- German Cancer Aid Foundation [70113343, 70114224]
- Hector Foundation [M20102]
- Helmholtz Zukunftsthema Ageing and Metabolic Programming [ZT0026]
- European Research Council (ERC) [101045416] Funding Source: European Research Council (ERC)
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CD8 agonism activates memory T cell metabolism and enhances the efficacy of memory T cell-based cancer immunotherapy.
Memory CD8(+) T cells mature after antigen clearance and ultimately express CD8 protein at levels higher than those detected in effector CD8(+) T cells. However, it is not clear whether engagement of CD8 in the absence of antigenic stimulation will result in the functional activation of T cells. Here, we found that CD8 antibody-mediated activation of memory CD8(+) T cells triggered T cell receptor (TCR) downstream signaling, enhanced T cell-mediated cytotoxicity and promoted effector cytokine production in a glucose- and glutamine-dependent manner. Furthermore, pretreatment of memory CD8(+) T cells with an agonistic anti-CD8 antibody enhanced their tumoricidal activity in vitro and in vivo. From these studies, we conclude that CD8 agonism activates glucose and glutamine metabolism in memory T cells and enhances the efficacy of memory T cell-based cancer immunotherapy.
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