期刊
INTERNATIONAL IMMUNOLOGY
卷 32, 期 7, 页码 485-491出版社
OXFORD UNIV PRESS
DOI: 10.1093/intimm/dxaa036
关键词
beta-catenin; fatty acid oxidation; indoleamine 2,3-dioxygenase; lipid bodies; PPAR
类别
资金
- Damon Runyon Foundation Physician Scientist Award
- National Institutes of Health (NIH) [K08 CA191063-04]
- Alliance for Cancer Gene Therapy Young Investigator Award
- Duke University Health Scholar Award
- Duke Strong Start Physician Scientist Award
The dendritic cell (DC) is recognized as a vital mediator of anti-tumor immunity. More recent studies have also demonstrated the important role of DCs in the generation of effective responses to checkpoint inhibitor immunotherapy. Metabolic programming of DCs dictates their functionality and can determine which DCs become immunostimulatory versus those that develop a tolerized phenotype capable of actively suppressing effector T-cell responses to cancers. As a result, there is great interest in understanding what mechanisms have evolved in cancers to alter these metabolic pathways, thereby allowing for their continued progression and metastasis. The therapeutic strategies developed to reverse these processes of DC tolerization in the tumor microenvironment represent promising candidates for future testing in combination immunotherapy clinical trials.
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