Hurdle or thruster: Glucose metabolism of T cells in anti-tumour immunity
Glucose metabolism is essential for the activation, differentiation and function of T cells and proper glucose metabolism is required to maintain effective T cell immunity. Dysregulation of glucose metabolism is a hallmark of cancer, and the tumour microenvironment (TME22TME: tumour microenvironment...
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Veröffentlicht in: | Biochimica et biophysica acta. Reviews on cancer 2024-01, Vol.1879 (1), p.189022-189022, Article 189022 |
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creator | Zhang, Sirui Zhang, Xiaozhen Yang, Hanshen Liang, Tingbo Bai, Xueli |
description | Glucose metabolism is essential for the activation, differentiation and function of T cells and proper glucose metabolism is required to maintain effective T cell immunity. Dysregulation of glucose metabolism is a hallmark of cancer, and the tumour microenvironment (TME22TME: tumour microenvironment.) can create metabolic barriers in T cells that inhibit their anti-tumour immune function. Targeting glucose metabolism is a promising approach to improve the capacity of T cells in the TME. The efficacy of common immunotherapies, such as immune checkpoint inhibitors (ICIs33ICI: immune checkpoint inhibitors.) and adoptive cell transfer (ACT44ACT: adoptive cell transfer therapy.), can be limited by T-cell function, and the treatment itself can affect T-cell metabolism. Therefore, understanding the relationship between immunotherapy and T cell glucose metabolism helps to achieve more effective anti-tumour therapy. In this review, we provide an overview of T cell glucose metabolism and how T cell metabolic reprogramming in the TME regulates anti-tumour responses, briefly describe the metabolic patterns of T cells during ICI and ACT therapies, which suggest possible synergistic strategies. |
doi_str_mv | 10.1016/j.bbcan.2023.189022 |
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Dysregulation of glucose metabolism is a hallmark of cancer, and the tumour microenvironment (TME22TME: tumour microenvironment.) can create metabolic barriers in T cells that inhibit their anti-tumour immune function. Targeting glucose metabolism is a promising approach to improve the capacity of T cells in the TME. The efficacy of common immunotherapies, such as immune checkpoint inhibitors (ICIs33ICI: immune checkpoint inhibitors.) and adoptive cell transfer (ACT44ACT: adoptive cell transfer therapy.), can be limited by T-cell function, and the treatment itself can affect T-cell metabolism. Therefore, understanding the relationship between immunotherapy and T cell glucose metabolism helps to achieve more effective anti-tumour therapy. 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Therefore, understanding the relationship between immunotherapy and T cell glucose metabolism helps to achieve more effective anti-tumour therapy. In this review, we provide an overview of T cell glucose metabolism and how T cell metabolic reprogramming in the TME regulates anti-tumour responses, briefly describe the metabolic patterns of T cells during ICI and ACT therapies, which suggest possible synergistic strategies.</description><subject>Adoptive cell transfer therapy</subject><subject>Glucose - metabolism</subject><subject>Humans</subject><subject>Immune checkpoint</subject><subject>Immunotherapy</subject><subject>Immunotherapy, Adoptive</subject><subject>Metabolic reprogramming</subject><subject>Neoplasms - metabolism</subject><subject>T cell</subject><subject>T-Lymphocytes</subject><subject>Tumor Microenvironment</subject><subject>Tumour microenvironment</subject><issn>0304-419X</issn><issn>1879-2561</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEtLxDAUhYMoOo7-AkGydNMxjzZpBBcivkBwM4K7kKZ3MEPbaB7C_Hs7dnTp6nLhnHvO_RA6o2RBCRWX60XTWDMsGGF8QWtFGNtDM1pLVbBK0H00I5yURUnV2xE6jnFNCK04F4foiEul-LjO0NNjDm0H2Aec3kOOCcIVfuiy9RFwD8k0vnOxx36Fl9hC10XsBmyG5IqUe58Ddn2fB5c2J-hgZboIp7s5R6_3d8vbx-L55eHp9ua5sLwqU0GlUaVkXBipqtXYgnFpqWm5ULKmleVM0YqQpuWqVRwEMaVsDDetYEoJCnyOLqa7H8F_ZohJ9y5um5kBfI6a1YqpUkiqRimfpDb4GAOs9EdwvQkbTYneMtRr_cNQbxnqieHoOt8F5KaH9s_zC20UXE8CGN_8chB0tA4GC60LYJNuvfs34BvLJoGO</recordid><startdate>202401</startdate><enddate>202401</enddate><creator>Zhang, Sirui</creator><creator>Zhang, Xiaozhen</creator><creator>Yang, Hanshen</creator><creator>Liang, Tingbo</creator><creator>Bai, Xueli</creator><general>Elsevier B.V</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>202401</creationdate><title>Hurdle or thruster: Glucose metabolism of T cells in anti-tumour immunity</title><author>Zhang, Sirui ; Zhang, Xiaozhen ; Yang, Hanshen ; Liang, Tingbo ; Bai, Xueli</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c354t-17a947236a795f930237c1ad3697815c3291500bd39d93e60a47ba3ad629961e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Adoptive cell transfer therapy</topic><topic>Glucose - metabolism</topic><topic>Humans</topic><topic>Immune checkpoint</topic><topic>Immunotherapy</topic><topic>Immunotherapy, Adoptive</topic><topic>Metabolic reprogramming</topic><topic>Neoplasms - metabolism</topic><topic>T cell</topic><topic>T-Lymphocytes</topic><topic>Tumor Microenvironment</topic><topic>Tumour microenvironment</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Sirui</creatorcontrib><creatorcontrib>Zhang, Xiaozhen</creatorcontrib><creatorcontrib>Yang, Hanshen</creatorcontrib><creatorcontrib>Liang, Tingbo</creatorcontrib><creatorcontrib>Bai, Xueli</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biochimica et biophysica acta. 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Dysregulation of glucose metabolism is a hallmark of cancer, and the tumour microenvironment (TME22TME: tumour microenvironment.) can create metabolic barriers in T cells that inhibit their anti-tumour immune function. Targeting glucose metabolism is a promising approach to improve the capacity of T cells in the TME. The efficacy of common immunotherapies, such as immune checkpoint inhibitors (ICIs33ICI: immune checkpoint inhibitors.) and adoptive cell transfer (ACT44ACT: adoptive cell transfer therapy.), can be limited by T-cell function, and the treatment itself can affect T-cell metabolism. Therefore, understanding the relationship between immunotherapy and T cell glucose metabolism helps to achieve more effective anti-tumour therapy. 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subjects | Adoptive cell transfer therapy Glucose - metabolism Humans Immune checkpoint Immunotherapy Immunotherapy, Adoptive Metabolic reprogramming Neoplasms - metabolism T cell T-Lymphocytes Tumor Microenvironment Tumour microenvironment |
title | Hurdle or thruster: Glucose metabolism of T cells in anti-tumour immunity |
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