Journal
NATURE IMMUNOLOGY
Volume 19, Issue 12, Pages 1319-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41590-018-0226-8
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Funding
- Deutsche Forschungsgemeinschaft (DFG) [SFB 1292]
- DFG [BO 3306/1-1, SCHM 1014/7-1, SCHM 1014/5-1, SFB 1066, TR SFB 156]
- Universitares Centrum fur Tumorerkrankungen
- Forschungszentrum Immuntherapie, core facility Histology, of the University Medical Center, Johannes Gutenberg University Mainz
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Many tumors evolve sophisticated strategies to evade the immune system, and these represent major obstacles for efficient antitumor immune responses. Here we explored a molecular mechanism of metabolic communication deployed by highly glycolytic tumors for immunoevasion. In contrast to colon adenocarcinomas, melanomas showed comparatively high glycolytic activity, which resulted in high acidification of the tumor microenvironment. This tumor acidosis induced Gprotein-coupled receptor-dependent expression of the transcriptional repressor ICER in tumor-associated macrophages that led to their functional polarization toward a non-inflammatory phenotype and promoted tumor growth. Collectively, our findings identify a molecular mechanism of metabolic communication between non-lymphoid tissue and the immune system that was exploited by high-glycolytic-rate tumors for evasion of the immune system.
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