文章基本信息

标题：Monocarboxylate transporter 1 deficiency impacts CD8 + T lymphocytes proliferation and recruitment to adipose tissue during obesity
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作者：C. Macchi ; A. Moregola ; M.F. Greco 等
期刊名称：iScience
印刷版ISSN：2589-0042
出版年度：2022
卷号：25
期号：6
页码：1-26
DOI：10.1016/j.isci.2022.104435
语种：English
出版社：Elsevier
摘要：SummaryLactate sits at the crossroad of metabolism, immunity, and inflammation. The expression of cellular lactate transporter MCT1 (known as Slc16a1) increases during immune cell activation to cope with the metabolic reprogramming. We investigated the impact of MCT1 deficiency on CD8+T cell function during obesity-related inflammatory conditions. The absence of MCT1 impaired CD8+T cell proliferation with a shift of ATP production to mitochondrial oxidative phosphorylation. InSlc16a1f/fTcellcremice fed a high-fat diet, a reduction in the number of CD8+T cells, which infiltrated epididymal visceral adipose tissue (epiWAT) or subcutaneous adipose tissue, was observed. Adipose tissue weight and adipocyte area were significantly reduced together with downregulation of adipogenic genes only in the epiWAT. Our findings highlight a distinct effect of MCT1 deficiency in CD8+T cells in the crosstalk with adipocytes and reinforce the concept that targeting immunometabolic reprogramming in lymphocyte could impact the immune-adipose tissue axis in obesity.Graphical abstractDisplay OmittedHighlights•MCT1 deficiency derails cell metabolism in activated CD8+T cells•MCT1 deficiency reduces cell proliferation of activated CD8+T cells•In obese mice, MCT1 deficiency reduces CD8+T effector cells infiltration in epiWAT•The lack of MCT1 in CD8+T cells leads to smaller adipocytes with a beiging phenotypeBiological sciences; Immunology; Metabolomics; Proteomics