Association of TIM-3 expression with glucose metabolism in Jurkat T cells
Abstract Background T cell activation is associated with increase in glycolysis and glutaminolysis. T cell immunoglobulin and mucin domain containing protein-3 (TIM-3), a T cell surface molecule, downregulates T cell activation and leads to insufficient immunity in cancer and chronic infection. TIM-...
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Format: | Article |
Language: | English |
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BMC
2020-08-01
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Series: | BMC Immunology |
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Online Access: | http://link.springer.com/article/10.1186/s12865-020-00377-6 |
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author | Mi Jin Lee Su Jin Yun Bokyoung Lee Eun Jeong Gyesoon Yoon Kyongmin Kim Sun Park |
author_facet | Mi Jin Lee Su Jin Yun Bokyoung Lee Eun Jeong Gyesoon Yoon Kyongmin Kim Sun Park |
author_sort | Mi Jin Lee |
collection | DOAJ |
description | Abstract Background T cell activation is associated with increase in glycolysis and glutaminolysis. T cell immunoglobulin and mucin domain containing protein-3 (TIM-3), a T cell surface molecule, downregulates T cell activation and leads to insufficient immunity in cancer and chronic infection. TIM-3 regulates T cell activation possibly through alterations in metabolism; however, the relationship between TIM-3 expression and T cell metabolic changes has not been well studied. Results We investigated the association between TIM-3 expression and metabolic changes by analyzing glucose metabolism, glutamine metabolism, and mitochondrial function in TIM-3 overexpressing or knockout Jurkat T cell lines relative to their control cell lines. Glucose uptake and consumption, and lactate release were downregulated by TIM-3 expression but upregulated by TIM-3 knockout. Concomitantly, the expression of the glucose transporter, Glut1, but not Glut2, 3, or 4 was altered by TIM-3 expression. However, TIM-3 expression alone could not account for the change in glutamine consumption, glutamate release, and mitochondrial mass, ROS production or membrane potential in these cell lines. Conclusion Our results show the association of TIM-3 expression with T cell glucose metabolism. These results are significant in chronic infections and cancers where it is necessary to control TIM-3 expressing T cells. |
first_indexed | 2024-12-19T22:59:13Z |
format | Article |
id | doaj.art-c1238df17744420d9ea5ff9a7a1f938b |
institution | Directory Open Access Journal |
issn | 1471-2172 |
language | English |
last_indexed | 2024-12-19T22:59:13Z |
publishDate | 2020-08-01 |
publisher | BMC |
record_format | Article |
series | BMC Immunology |
spelling | doaj.art-c1238df17744420d9ea5ff9a7a1f938b2022-12-21T20:02:34ZengBMCBMC Immunology1471-21722020-08-0121111310.1186/s12865-020-00377-6Association of TIM-3 expression with glucose metabolism in Jurkat T cellsMi Jin Lee0Su Jin Yun1Bokyoung Lee2Eun Jeong3Gyesoon Yoon4Kyongmin Kim5Sun Park6Department of Microbiology, Ajou University School of MedicineDepartment of Microbiology, Ajou University School of MedicineDepartment of Microbiology, Ajou University School of MedicineDepartment of Microbiology, Ajou University School of MedicineDepartment of Biochemistry & Molecular Biology, Ajou University School of MedicineDepartment of Microbiology, Ajou University School of MedicineDepartment of Microbiology, Ajou University School of MedicineAbstract Background T cell activation is associated with increase in glycolysis and glutaminolysis. T cell immunoglobulin and mucin domain containing protein-3 (TIM-3), a T cell surface molecule, downregulates T cell activation and leads to insufficient immunity in cancer and chronic infection. TIM-3 regulates T cell activation possibly through alterations in metabolism; however, the relationship between TIM-3 expression and T cell metabolic changes has not been well studied. Results We investigated the association between TIM-3 expression and metabolic changes by analyzing glucose metabolism, glutamine metabolism, and mitochondrial function in TIM-3 overexpressing or knockout Jurkat T cell lines relative to their control cell lines. Glucose uptake and consumption, and lactate release were downregulated by TIM-3 expression but upregulated by TIM-3 knockout. Concomitantly, the expression of the glucose transporter, Glut1, but not Glut2, 3, or 4 was altered by TIM-3 expression. However, TIM-3 expression alone could not account for the change in glutamine consumption, glutamate release, and mitochondrial mass, ROS production or membrane potential in these cell lines. Conclusion Our results show the association of TIM-3 expression with T cell glucose metabolism. These results are significant in chronic infections and cancers where it is necessary to control TIM-3 expressing T cells.http://link.springer.com/article/10.1186/s12865-020-00377-6HAVCR2GlycolysisCD4+ T cellGlutaminolysisGlucose transporter |
spellingShingle | Mi Jin Lee Su Jin Yun Bokyoung Lee Eun Jeong Gyesoon Yoon Kyongmin Kim Sun Park Association of TIM-3 expression with glucose metabolism in Jurkat T cells BMC Immunology HAVCR2 Glycolysis CD4+ T cell Glutaminolysis Glucose transporter |
title | Association of TIM-3 expression with glucose metabolism in Jurkat T cells |
title_full | Association of TIM-3 expression with glucose metabolism in Jurkat T cells |
title_fullStr | Association of TIM-3 expression with glucose metabolism in Jurkat T cells |
title_full_unstemmed | Association of TIM-3 expression with glucose metabolism in Jurkat T cells |
title_short | Association of TIM-3 expression with glucose metabolism in Jurkat T cells |
title_sort | association of tim 3 expression with glucose metabolism in jurkat t cells |
topic | HAVCR2 Glycolysis CD4+ T cell Glutaminolysis Glucose transporter |
url | http://link.springer.com/article/10.1186/s12865-020-00377-6 |
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