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Nojima, Ichiro Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Eikawa, Shingo Department of Hematology/Oncology, Hess Cancer Institute, Icahn School of Medicine At Mount Sinai Kaken ID
Tomonobu, Nahoko Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Hada, Yoshiko Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Kajitani, Nobuo Department of Internal Medicine, Diabetes Center, Okayama City Hospital
Teshigawara, Sanae Diabetes Center, Okayama S
Miyamoto, Satoshi Center for Innovative Clinical Medicine, Okayama University Hospital Kaken ID
Tone, Atsuhito Diabetes Center, Okayama Saiseikai General Hospital
Uchida, Haruhito A. Department of Chronic Kidney Disease and Cardiovascular Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Nakatsuka, Atsuko Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Kaken ID publons researchmap
Eguchi, Jun Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Kaken ID researchmap
Shikata, Kenichi Center for Innovative Clinical Medicine, Okayama University Hospital ORCID Kaken ID publons researchmap
Udono, Heiichiro Department of Immunology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Kaken ID researchmap
Wada, Jun Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences ORCID Kaken ID publons researchmap
Abstract
The metabolic changes and dysfunction in CD8+T cells may be involved in tumor progression and susceptibility to virus infection in type 2 diabetes (T2D). In C57BL/6JJcl mice fed with high fat-high sucrose chow (HFS), multifunctionality of CD8+splenic and tumor-infiltrating lymphocytes (TILs) was impaired and associated with enhanced tumor growth, which were inhibited by metformin. In CD8+splenic T cells from the HFS mice, glycolysis/basal respiration ratio was significantly reduced and reversed by metformin. In the patients with T2D (DM), multifunctionality of circulating CD8+PD-1+T cells stimulated with PMA/ionomycin as well as with HLA-A*24:02 CMV peptide was dampened, while metformin recovered multifunctionality. Both glycolysis and basal respiration were reduced in DM, and glycolysis was increased by metformin. The disturbance of the link between metabolism and immune function in CD8+PD-1+T cells in T2D was proved by recovery of antigen-specific and non-specific cytokine production via metformin-mediated increase in glycolytic activity.
Keywords
Cytokines
Diabetes
Endocrine system and metabolic diseases
Immunology
Tumour immunology
Published Date
2020-09-10
Publication Title
Scientific Reports
Volume
volume10
Issue
issue1
Publisher
Nature Research
Start Page
14928
ISSN
2045-2322
Content Type
Journal Article
language
英語
OAI-PMH Set
岡山大学
Copyright Holders
© The Author(s) 2020
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PubMed ID
DOI
Web of Science KeyUT
Related Url
isVersionOf https://doi.org/10.1038/s41598-020-71946-3
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http://creat iveco mmons .org/licen ses/by/4.0/
Funder Name
Japan Society for the Promotion of Science
助成番号
19H03675