Accumulation of long-chain fatty acids in the tumor microenvironment drives dysfunction in intrapancreatic CD8+ T cells

CD8+ T cells are master effectors of antitumor immunity, and their presence at tumor sites correlates with favorable outcomes. However, metabolic constraints imposed by the tumor microenvironment (TME) can dampen their ability to control tumor progression. We describe lipid accumulation in the TME a...

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Veröffentlicht in:The Journal of experimental medicine Jg. 217; H. 8
Hauptverfasser: Manzo, Teresa, Prentice, Boone M, Anderson, Kristin G, Raman, Ayush, Schalck, Aislyn, Codreanu, Gabriela S, Nava Lauson, Carina B, Tiberti, Silvia, Raimondi, Andrea, Jones, Marissa A, Reyzer, Michelle, Bates, Breanna M, Spraggins, Jeffrey M, Patterson, Nathan H, McLean, John A, Rai, Kunal, Tacchetti, Carlo, Tucci, Sara, Wargo, Jennifer A, Rodighiero, Simona, Clise-Dwyer, Karen, Sherrod, Stacy D, Kim, Michael, Navin, Nicholas E, Caprioli, Richard M, Greenberg, Philip D, Draetta, Giulio, Nezi, Luigi
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 03.08.2020
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ISSN:1540-9538, 1540-9538
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Abstract CD8+ T cells are master effectors of antitumor immunity, and their presence at tumor sites correlates with favorable outcomes. However, metabolic constraints imposed by the tumor microenvironment (TME) can dampen their ability to control tumor progression. We describe lipid accumulation in the TME areas of pancreatic ductal adenocarcinoma (PDA) populated by CD8+ T cells infiltrating both murine and human tumors. In this lipid-rich but otherwise nutrient-poor TME, access to using lipid metabolism becomes particularly valuable for sustaining cell functions. Here, we found that intrapancreatic CD8+ T cells progressively accumulate specific long-chain fatty acids (LCFAs), which, rather than provide a fuel source, impair their mitochondrial function and trigger major transcriptional reprogramming of pathways involved in lipid metabolism, with the subsequent reduction of fatty acid catabolism. In particular, intrapancreatic CD8+ T cells specifically exhibit down-regulation of the very-long-chain acyl-CoA dehydrogenase (VLCAD) enzyme, which exacerbates accumulation of LCFAs and very-long-chain fatty acids (VLCFAs) that mediate lipotoxicity. Metabolic reprogramming of tumor-specific T cells through enforced expression of ACADVL enabled enhanced intratumoral T cell survival and persistence in an engineered mouse model of PDA, overcoming one of the major hurdles to immunotherapy for PDA.
AbstractList CD8+ T cells are master effectors of antitumor immunity, and their presence at tumor sites correlates with favorable outcomes. However, metabolic constraints imposed by the tumor microenvironment (TME) can dampen their ability to control tumor progression. We describe lipid accumulation in the TME areas of pancreatic ductal adenocarcinoma (PDA) populated by CD8+ T cells infiltrating both murine and human tumors. In this lipid-rich but otherwise nutrient-poor TME, access to using lipid metabolism becomes particularly valuable for sustaining cell functions. Here, we found that intrapancreatic CD8+ T cells progressively accumulate specific long-chain fatty acids (LCFAs), which, rather than provide a fuel source, impair their mitochondrial function and trigger major transcriptional reprogramming of pathways involved in lipid metabolism, with the subsequent reduction of fatty acid catabolism. In particular, intrapancreatic CD8+ T cells specifically exhibit down-regulation of the very-long-chain acyl-CoA dehydrogenase (VLCAD) enzyme, which exacerbates accumulation of LCFAs and very-long-chain fatty acids (VLCFAs) that mediate lipotoxicity. Metabolic reprogramming of tumor-specific T cells through enforced expression of ACADVL enabled enhanced intratumoral T cell survival and persistence in an engineered mouse model of PDA, overcoming one of the major hurdles to immunotherapy for PDA.
CD8+ T cells are master effectors of antitumor immunity, and their presence at tumor sites correlates with favorable outcomes. However, metabolic constraints imposed by the tumor microenvironment (TME) can dampen their ability to control tumor progression. We describe lipid accumulation in the TME areas of pancreatic ductal adenocarcinoma (PDA) populated by CD8+ T cells infiltrating both murine and human tumors. In this lipid-rich but otherwise nutrient-poor TME, access to using lipid metabolism becomes particularly valuable for sustaining cell functions. Here, we found that intrapancreatic CD8+ T cells progressively accumulate specific long-chain fatty acids (LCFAs), which, rather than provide a fuel source, impair their mitochondrial function and trigger major transcriptional reprogramming of pathways involved in lipid metabolism, with the subsequent reduction of fatty acid catabolism. In particular, intrapancreatic CD8+ T cells specifically exhibit down-regulation of the very-long-chain acyl-CoA dehydrogenase (VLCAD) enzyme, which exacerbates accumulation of LCFAs and very-long-chain fatty acids (VLCFAs) that mediate lipotoxicity. Metabolic reprogramming of tumor-specific T cells through enforced expression of ACADVL enabled enhanced intratumoral T cell survival and persistence in an engineered mouse model of PDA, overcoming one of the major hurdles to immunotherapy for PDA.CD8+ T cells are master effectors of antitumor immunity, and their presence at tumor sites correlates with favorable outcomes. However, metabolic constraints imposed by the tumor microenvironment (TME) can dampen their ability to control tumor progression. We describe lipid accumulation in the TME areas of pancreatic ductal adenocarcinoma (PDA) populated by CD8+ T cells infiltrating both murine and human tumors. In this lipid-rich but otherwise nutrient-poor TME, access to using lipid metabolism becomes particularly valuable for sustaining cell functions. Here, we found that intrapancreatic CD8+ T cells progressively accumulate specific long-chain fatty acids (LCFAs), which, rather than provide a fuel source, impair their mitochondrial function and trigger major transcriptional reprogramming of pathways involved in lipid metabolism, with the subsequent reduction of fatty acid catabolism. In particular, intrapancreatic CD8+ T cells specifically exhibit down-regulation of the very-long-chain acyl-CoA dehydrogenase (VLCAD) enzyme, which exacerbates accumulation of LCFAs and very-long-chain fatty acids (VLCFAs) that mediate lipotoxicity. Metabolic reprogramming of tumor-specific T cells through enforced expression of ACADVL enabled enhanced intratumoral T cell survival and persistence in an engineered mouse model of PDA, overcoming one of the major hurdles to immunotherapy for PDA.
Author Bates, Breanna M
Raimondi, Andrea
Caprioli, Richard M
Tucci, Sara
Raman, Ayush
Kim, Michael
Patterson, Nathan H
Jones, Marissa A
McLean, John A
Tacchetti, Carlo
Sherrod, Stacy D
Clise-Dwyer, Karen
Tiberti, Silvia
Schalck, Aislyn
Wargo, Jennifer A
Anderson, Kristin G
Codreanu, Gabriela S
Manzo, Teresa
Rai, Kunal
Navin, Nicholas E
Nava Lauson, Carina B
Greenberg, Philip D
Reyzer, Michelle
Rodighiero, Simona
Prentice, Boone M
Nezi, Luigi
Draetta, Giulio
Spraggins, Jeffrey M
Author_xml – sequence: 1
  givenname: Teresa
  surname: Manzo
  fullname: Manzo, Teresa
  organization: Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX
– sequence: 2
  givenname: Boone M
  surname: Prentice
  fullname: Prentice, Boone M
  organization: Department of Biochemistry, Mass Spectrometry Research Center, Department of Chemistry, Department of Pharmacology and Medicine, Vanderbilt University, Nashville, TN
– sequence: 3
  givenname: Kristin G
  surname: Anderson
  fullname: Anderson, Kristin G
  organization: Departments of Medicine/Oncology and Immunology, University of Washington School of Medicine, Seattle, WA
– sequence: 4
  givenname: Ayush
  surname: Raman
  fullname: Raman, Ayush
  organization: Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX
– sequence: 5
  givenname: Aislyn
  surname: Schalck
  fullname: Schalck, Aislyn
  organization: Department of Genetics and Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX
– sequence: 6
  givenname: Gabriela S
  surname: Codreanu
  fullname: Codreanu, Gabriela S
  organization: Center for Innovative Technology, Vanderbilt University, Nashville, TN
– sequence: 7
  givenname: Carina B
  surname: Nava Lauson
  fullname: Nava Lauson, Carina B
  organization: Department of Experimental Oncology, IRCCS European Institute of Oncology, Milano, Italy
– sequence: 8
  givenname: Silvia
  surname: Tiberti
  fullname: Tiberti, Silvia
  organization: Department of Experimental Oncology, IRCCS European Institute of Oncology, Milano, Italy
– sequence: 9
  givenname: Andrea
  surname: Raimondi
  fullname: Raimondi, Andrea
  organization: Experimental Imaging Center, IRCCS San Raffaele Scientific Institute, San Raffaele Vita-Salute University, Milano, Italy
– sequence: 10
  givenname: Marissa A
  surname: Jones
  fullname: Jones, Marissa A
  organization: Department of Biochemistry, Mass Spectrometry Research Center, Department of Chemistry, Department of Pharmacology and Medicine, Vanderbilt University, Nashville, TN
– sequence: 11
  givenname: Michelle
  surname: Reyzer
  fullname: Reyzer, Michelle
  organization: Department of Biochemistry, Mass Spectrometry Research Center, Department of Chemistry, Department of Pharmacology and Medicine, Vanderbilt University, Nashville, TN
– sequence: 12
  givenname: Breanna M
  surname: Bates
  fullname: Bates, Breanna M
  organization: Departments of Medicine/Oncology and Immunology, University of Washington School of Medicine, Seattle, WA
– sequence: 13
  givenname: Jeffrey M
  surname: Spraggins
  fullname: Spraggins, Jeffrey M
  organization: Department of Biochemistry, Mass Spectrometry Research Center, Department of Chemistry, Department of Pharmacology and Medicine, Vanderbilt University, Nashville, TN
– sequence: 14
  givenname: Nathan H
  surname: Patterson
  fullname: Patterson, Nathan H
  organization: Department of Biochemistry, Mass Spectrometry Research Center, Department of Chemistry, Department of Pharmacology and Medicine, Vanderbilt University, Nashville, TN
– sequence: 15
  givenname: John A
  surname: McLean
  fullname: McLean, John A
  organization: Center for Innovative Technology, Vanderbilt University, Nashville, TN
– sequence: 16
  givenname: Kunal
  surname: Rai
  fullname: Rai, Kunal
  organization: Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX
– sequence: 17
  givenname: Carlo
  surname: Tacchetti
  fullname: Tacchetti, Carlo
  organization: Experimental Imaging Center, IRCCS San Raffaele Scientific Institute, San Raffaele Vita-Salute University, Milano, Italy
– sequence: 18
  givenname: Sara
  surname: Tucci
  fullname: Tucci, Sara
  organization: Laboratory of Clinical Biochemistry and Metabolism Center for Pediatrics and Adolescent Medicine, University of Freiburg, Freiburg, Germany
– sequence: 19
  givenname: Jennifer A
  surname: Wargo
  fullname: Wargo, Jennifer A
  organization: Department of Surgical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX
– sequence: 20
  givenname: Simona
  surname: Rodighiero
  fullname: Rodighiero, Simona
  organization: Department of Experimental Oncology, IRCCS European Institute of Oncology, Milano, Italy
– sequence: 21
  givenname: Karen
  surname: Clise-Dwyer
  fullname: Clise-Dwyer, Karen
  organization: Department of Stem Cell Transplantation, The University of Texas MD Anderson Cancer Center, Houston, TX
– sequence: 22
  givenname: Stacy D
  surname: Sherrod
  fullname: Sherrod, Stacy D
  organization: Center for Innovative Technology, Vanderbilt University, Nashville, TN
– sequence: 23
  givenname: Michael
  surname: Kim
  fullname: Kim, Michael
  organization: Department of Surgical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX
– sequence: 24
  givenname: Nicholas E
  surname: Navin
  fullname: Navin, Nicholas E
  organization: Department of Genetics and Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX
– sequence: 25
  givenname: Richard M
  surname: Caprioli
  fullname: Caprioli, Richard M
  organization: Department of Biochemistry, Mass Spectrometry Research Center, Department of Chemistry, Department of Pharmacology and Medicine, Vanderbilt University, Nashville, TN
– sequence: 26
  givenname: Philip D
  surname: Greenberg
  fullname: Greenberg, Philip D
  organization: Departments of Medicine/Oncology and Immunology, University of Washington School of Medicine, Seattle, WA
– sequence: 27
  givenname: Giulio
  surname: Draetta
  fullname: Draetta, Giulio
  organization: Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX
– sequence: 28
  givenname: Luigi
  surname: Nezi
  fullname: Nezi, Luigi
  organization: Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX
BackLink https://www.ncbi.nlm.nih.gov/pubmed/32491160$$D View this record in MEDLINE/PubMed
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Snippet CD8+ T cells are master effectors of antitumor immunity, and their presence at tumor sites correlates with favorable outcomes. However, metabolic constraints...
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SubjectTerms Acyl-CoA Dehydrogenase, Long-Chain - biosynthesis
Acyl-CoA Dehydrogenase, Long-Chain - genetics
Animals
Carcinoma, Pancreatic Ductal - genetics
Carcinoma, Pancreatic Ductal - metabolism
Carcinoma, Pancreatic Ductal - pathology
CD8-Positive T-Lymphocytes - metabolism
CD8-Positive T-Lymphocytes - pathology
Down-Regulation
Fatty Acids - genetics
Fatty Acids - metabolism
Gene Expression Regulation, Enzymologic
Gene Expression Regulation, Neoplastic
Lymphocytes, Tumor-Infiltrating - metabolism
Lymphocytes, Tumor-Infiltrating - pathology
Mice
Mice, Mutant Strains
Neoplasm Proteins - biosynthesis
Neoplasm Proteins - genetics
Pancreas - metabolism
Pancreas - pathology
Pancreatic Neoplasms - genetics
Pancreatic Neoplasms - metabolism
Pancreatic Neoplasms - pathology
Tumor Microenvironment
Title Accumulation of long-chain fatty acids in the tumor microenvironment drives dysfunction in intrapancreatic CD8+ T cells
URI https://www.ncbi.nlm.nih.gov/pubmed/32491160
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