γδ T Cells Support Pancreatic Oncogenesis by Restraining αβ T Cell Activation
Inflammation is paramount in pancreatic oncogenesis. We identified a uniquely activated γδT cell population, which constituted ∼40% of tumor-infiltrating T cells in human pancreatic ductal adenocarcinoma (PDA). Recruitment and activation of γδT cells was contingent on diverse chemokine signals. Dele...
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| Published in | Cell Vol. 166; no. 6; pp. 1485 - 1499.e15 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
08.09.2016
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Inflammation is paramount in pancreatic oncogenesis. We identified a uniquely activated γδT cell population, which constituted ∼40% of tumor-infiltrating T cells in human pancreatic ductal adenocarcinoma (PDA). Recruitment and activation of γδT cells was contingent on diverse chemokine signals. Deletion, depletion, or blockade of γδT cell recruitment was protective against PDA and resulted in increased infiltration, activation, and Th1 polarization of αβT cells. Although αβT cells were dispensable to outcome in PDA, they became indispensable mediators of tumor protection upon γδT cell ablation. PDA-infiltrating γδT cells expressed high levels of exhaustion ligands and thereby negated adaptive anti-tumor immunity. Blockade of PD-L1 in γδT cells enhanced CD4+ and CD8+ T cell infiltration and immunogenicity and induced tumor protection suggesting that γδT cells are critical sources of immune-suppressive checkpoint ligands in PDA. We describe γδT cells as central regulators of effector T cell activation in cancer via novel cross-talk.
[Display omitted]
•γδT cells are highly prevalent in human pancreatic carcinoma•Deletion or interruption of γδT cell recruitment is protective in pancreatic cancer•Pancreatic cancer infiltrating γδT cells express high levels of checkpoint ligands•γδT cells disable αβT cell activation via checkpoint receptor ligation
γδT cells are key regulators of effector T cell activation in pancreatic cancer and a new target for cancer immunotherapy. |
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| AbstractList | Inflammation is paramount in pancreatic oncogenesis. We identified a uniquely activated γδT cell population, which constituted ∼40% of tumor-infiltrating T cells in human pancreatic ductal adenocarcinoma (PDA). Recruitment and activation of γδT cells was contingent on diverse chemokine signals. Deletion, depletion, or blockade of γδT cell recruitment was protective against PDA and resulted in increased infiltration, activation, and Th1 polarization of αβT cells. Although αβT cells were dispensable to outcome in PDA, they became indispensable mediators of tumor protection upon γδT cell ablation. PDA-infiltrating γδT cells expressed high levels of exhaustion ligands and thereby negated adaptive anti-tumor immunity. Blockade of PD-L1 in γδT cells enhanced CD4(+) and CD8(+) T cell infiltration and immunogenicity and induced tumor protection suggesting that γδT cells are critical sources of immune-suppressive checkpoint ligands in PDA. We describe γδT cells as central regulators of effector T cell activation in cancer via novel cross-talk.Inflammation is paramount in pancreatic oncogenesis. We identified a uniquely activated γδT cell population, which constituted ∼40% of tumor-infiltrating T cells in human pancreatic ductal adenocarcinoma (PDA). Recruitment and activation of γδT cells was contingent on diverse chemokine signals. Deletion, depletion, or blockade of γδT cell recruitment was protective against PDA and resulted in increased infiltration, activation, and Th1 polarization of αβT cells. Although αβT cells were dispensable to outcome in PDA, they became indispensable mediators of tumor protection upon γδT cell ablation. PDA-infiltrating γδT cells expressed high levels of exhaustion ligands and thereby negated adaptive anti-tumor immunity. Blockade of PD-L1 in γδT cells enhanced CD4(+) and CD8(+) T cell infiltration and immunogenicity and induced tumor protection suggesting that γδT cells are critical sources of immune-suppressive checkpoint ligands in PDA. We describe γδT cells as central regulators of effector T cell activation in cancer via novel cross-talk. Inflammation is paramount in pancreatic oncogenesis. We identified a uniquely activated γδT cell population, which constituted ∼40% of tumor-infiltrating T cells in human pancreatic ductal adenocarcinoma (PDA). Recruitment and activation of γδT cells was contingent on diverse chemokine signals. Deletion, depletion, or blockade of γδT cell recruitment was protective against PDA and resulted in increased infiltration, activation, and Th1 polarization of αβT cells. Although αβT cells were dispensable to outcome in PDA, they became indispensable mediators of tumor protection upon γδT cell ablation. PDA-infiltrating γδT cells expressed high levels of exhaustion ligands and thereby negated adaptive anti-tumor immunity. Blockade of PD-L1 in γδT cells enhanced CD4⁺ and CD8⁺ T cell infiltration and immunogenicity and induced tumor protection suggesting that γδT cells are critical sources of immune-suppressive checkpoint ligands in PDA. We describe γδT cells as central regulators of effector T cell activation in cancer via novel cross-talk. Inflammation is paramount in pancreatic oncogenesis. We identified a uniquely activated γδT cell population, which constituted ∼40% of tumor-infiltrating T cells in human pancreatic ductal adenocarcinoma (PDA). Recruitment and activation of γδT cells was contingent on diverse chemokine signals. Deletion, depletion, or blockade of γδT cell recruitment was protective against PDA and resulted in increased infiltration, activation, and Th1 polarization of αβT cells. Although αβT cells were dispensable to outcome in PDA, they became indispensable mediators of tumor protection upon γδT cell ablation. PDA-infiltrating γδT cells expressed high levels of exhaustion ligands and thereby negated adaptive anti-tumor immunity. Blockade of PD-L1 in γδT cells enhanced CD4+ and CD8+ T cell infiltration and immunogenicity and induced tumor protection suggesting that γδT cells are critical sources of immune-suppressive checkpoint ligands in PDA. We describe γδT cells as central regulators of effector T cell activation in cancer via novel cross-talk. [Display omitted] •γδT cells are highly prevalent in human pancreatic carcinoma•Deletion or interruption of γδT cell recruitment is protective in pancreatic cancer•Pancreatic cancer infiltrating γδT cells express high levels of checkpoint ligands•γδT cells disable αβT cell activation via checkpoint receptor ligation γδT cells are key regulators of effector T cell activation in pancreatic cancer and a new target for cancer immunotherapy. Inflammation is paramount in pancreatic oncogenesis. We identified a uniquely-activated γδT cell population which constituted ∼40% of tumor-infiltrating T cells in human pancreatic ductal adenocarcinoma (PDA). Recruitment and activation of γδT cells was contingent on diverse chemokine signals. Deletion, depletion, or blockade of γδT cell recruitment was protective against PDA and resulted in increased infiltration, activation, and Th1-polarization of αβT cells. Whereas αβT cells were dispensable to outcome in PDA, they became indispensable mediators of tumor-protection upon γδT cell ablation. PDA-infiltrating γδT cells expressed high levels of exhaustion ligands and thereby negated adaptive anti-tumor immunity. Blockade of PD-L1 in γδT cells enhanced CD4 + and CD8 + T cell infiltration and immunogenicity and induced tumor-protection suggesting that γδT cells are critical sources of immune-suppressive checkpoint ligands in PDA. We describe γδT cells as central regulators of effector T cell activation in cancer via novel cross-talk. γδT cells are key regulators of effector T cell activation in pancreatic cancer and a new target for cancer immunotherapy Inflammation is paramount in pancreatic oncogenesis. We identified a uniquely activated γδT cell population, which constituted ∼40% of tumor-infiltrating T cells in human pancreatic ductal adenocarcinoma (PDA). Recruitment and activation of γδT cells was contingent on diverse chemokine signals. Deletion, depletion, or blockade of γδT cell recruitment was protective against PDA and resulted in increased infiltration, activation, and Th1 polarization of αβT cells. Although αβT cells were dispensable to outcome in PDA, they became indispensable mediators of tumor protection upon γδT cell ablation. PDA-infiltrating γδT cells expressed high levels of exhaustion ligands and thereby negated adaptive anti-tumor immunity. Blockade of PD-L1 in γδT cells enhanced CD4(+) and CD8(+) T cell infiltration and immunogenicity and induced tumor protection suggesting that γδT cells are critical sources of immune-suppressive checkpoint ligands in PDA. We describe γδT cells as central regulators of effector T cell activation in cancer via novel cross-talk. |
| Author | Narayanan, Rajkishen Hundeyin, Mautin Newman, Elliot Miller, George Zambirinis, Constantinos Pantelis Torres-Hernandez, Alejandro Seifert, Lena Dustin, Michael Loran Daley, Donnele Mani, Vishnu Raj Kumar Hajdu, Cristina Akkad, Neha Jang, Jung-Eun Barilla, Rocky Mohan, Navyatha Avanzi, Antonina Pillarisetty, Venu Gopal Bar-Sagi, Dafna Werba, Gregor Tippens, Daniel |
| AuthorAffiliation | 5 The Kennedy Institute of Rheumatology, University of Oxford, Roosevelt Drive, Headington Oxford, OX3 7FY, United Kingdom 1 S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, 430 East 29th Street, New York, NY 10016 6 S. Arthur Localio Laboratory, Department of Cell Biology, New York University School of Medicine, 430 East 29th Street, New York, NY 10016 2 S. Arthur Localio Laboratory, Department of Biochemistry, New York University School of Medicine, 430 East 29th Street, New York, NY 10016 3 S. Arthur Localio Laboratory, Department of Pathology, New York University School of Medicine, 430 East 29th Street, New York, NY 10016 4 Department of Surgery, University of Washington School of Medicine, 1959 NE Pacific St, Seattle, WA 98195 |
| AuthorAffiliation_xml | – name: 5 The Kennedy Institute of Rheumatology, University of Oxford, Roosevelt Drive, Headington Oxford, OX3 7FY, United Kingdom – name: 2 S. Arthur Localio Laboratory, Department of Biochemistry, New York University School of Medicine, 430 East 29th Street, New York, NY 10016 – name: 6 S. Arthur Localio Laboratory, Department of Cell Biology, New York University School of Medicine, 430 East 29th Street, New York, NY 10016 – name: 3 S. Arthur Localio Laboratory, Department of Pathology, New York University School of Medicine, 430 East 29th Street, New York, NY 10016 – name: 4 Department of Surgery, University of Washington School of Medicine, 1959 NE Pacific St, Seattle, WA 98195 – name: 1 S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, 430 East 29th Street, New York, NY 10016 |
| Author_xml | – sequence: 1 givenname: Donnele surname: Daley fullname: Daley, Donnele organization: S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, 430 East 29th Street, New York, NY 10016, USA – sequence: 2 givenname: Constantinos Pantelis surname: Zambirinis fullname: Zambirinis, Constantinos Pantelis organization: S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, 430 East 29th Street, New York, NY 10016, USA – sequence: 3 givenname: Lena surname: Seifert fullname: Seifert, Lena organization: S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, 430 East 29th Street, New York, NY 10016, USA – sequence: 4 givenname: Neha surname: Akkad fullname: Akkad, Neha organization: S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, 430 East 29th Street, New York, NY 10016, USA – sequence: 5 givenname: Navyatha surname: Mohan fullname: Mohan, Navyatha organization: S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, 430 East 29th Street, New York, NY 10016, USA – sequence: 6 givenname: Gregor surname: Werba fullname: Werba, Gregor organization: S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, 430 East 29th Street, New York, NY 10016, USA – sequence: 7 givenname: Rocky surname: Barilla fullname: Barilla, Rocky organization: S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, 430 East 29th Street, New York, NY 10016, USA – sequence: 8 givenname: Alejandro surname: Torres-Hernandez fullname: Torres-Hernandez, Alejandro organization: S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, 430 East 29th Street, New York, NY 10016, USA – sequence: 9 givenname: Mautin surname: Hundeyin fullname: Hundeyin, Mautin organization: S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, 430 East 29th Street, New York, NY 10016, USA – sequence: 10 givenname: Vishnu Raj Kumar surname: Mani fullname: Mani, Vishnu Raj Kumar organization: S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, 430 East 29th Street, New York, NY 10016, USA – sequence: 11 givenname: Antonina surname: Avanzi fullname: Avanzi, Antonina organization: S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, 430 East 29th Street, New York, NY 10016, USA – sequence: 12 givenname: Daniel surname: Tippens fullname: Tippens, Daniel organization: S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, 430 East 29th Street, New York, NY 10016, USA – sequence: 13 givenname: Rajkishen surname: Narayanan fullname: Narayanan, Rajkishen organization: S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, 430 East 29th Street, New York, NY 10016, USA – sequence: 14 givenname: Jung-Eun surname: Jang fullname: Jang, Jung-Eun organization: Department of Biochemistry, New York University School of Medicine, 430 East 29th Street, New York, NY 10016, USA – sequence: 15 givenname: Elliot surname: Newman fullname: Newman, Elliot organization: S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, 430 East 29th Street, New York, NY 10016, USA – sequence: 16 givenname: Venu Gopal surname: Pillarisetty fullname: Pillarisetty, Venu Gopal organization: Department of Surgery, University of Washington School of Medicine, 1959 NE Pacific Street, Seattle, WA 98195, USA – sequence: 17 givenname: Michael Loran surname: Dustin fullname: Dustin, Michael Loran organization: Department of Pathology, New York University School of Medicine, 430 East 29th Street, New York, NY 10016, USA – sequence: 18 givenname: Dafna surname: Bar-Sagi fullname: Bar-Sagi, Dafna organization: Department of Biochemistry, New York University School of Medicine, 430 East 29th Street, New York, NY 10016, USA – sequence: 19 givenname: Cristina surname: Hajdu fullname: Hajdu, Cristina organization: Department of Pathology, New York University School of Medicine, 430 East 29th Street, New York, NY 10016, USA – sequence: 20 givenname: George surname: Miller fullname: Miller, George email: george.miller@nyumc.org organization: S. Arthur Localio Laboratory, Department of Surgery, New York University School of Medicine, 430 East 29th Street, New York, NY 10016, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27569912$$D View this record in MEDLINE/PubMed |
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| Snippet | Inflammation is paramount in pancreatic oncogenesis. We identified a uniquely activated γδT cell population, which constituted ∼40% of tumor-infiltrating... Inflammation is paramount in pancreatic oncogenesis. We identified a uniquely activated γδT cell population, which constituted ∼40% of tumor-infiltrating T... Inflammation is paramount in pancreatic oncogenesis. We identified a uniquely-activated γδT cell population which constituted ∼40% of tumor-infiltrating T... |
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| SubjectTerms | Adaptive Immunity adenocarcinoma Animals cancer carcinogenesis Carcinogenesis - immunology Carcinogenesis - pathology Carcinoma, Pancreatic Ductal - immunology Carcinoma, Pancreatic Ductal - physiopathology CD8-positive T-lymphocytes Cells, Cultured checkpoint ligands chemokines Chemokines - immunology Epithelial Cells - physiology Female Humans immune response inflammation Kras Ligands Lymphocyte Activation - immunology Male Mice Mice, Inbred C57BL Signal Transduction - immunology T-Lymphocytes - immunology Tumor Microenvironment - immunology |
| Title | γδ T Cells Support Pancreatic Oncogenesis by Restraining αβ T Cell Activation |
| URI | https://dx.doi.org/10.1016/j.cell.2016.07.046 https://www.ncbi.nlm.nih.gov/pubmed/27569912 https://www.proquest.com/docview/1818339710 https://www.proquest.com/docview/2000223835 https://pubmed.ncbi.nlm.nih.gov/PMC5017923 |
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