Characterization of the effect of a GLUT1 inhibitor on macrophages and T cells for modulating the immune response to myocardial infarction

The intricate relationship between glucose metabolism and immune cell function, with a specific focus on the role of the glucose transporter-1 (GLUT1), is crucial in modulating T cells and macrophages. Through a series of extensive in vitro experiments, this work aims to elucidate the effects of BAY-876, the specific GLUT1 inhibitor, on these immune cell populations and assess its potential as a therapeutic agent in immune modulation. The here presented study utilized primary T cells and macrophages to explore the impact of BAY-876 on key immune cell functions. The results demonstrated that BAY- 876 treatment led to a significant reduction in glucose uptake and lactate production in T cells, indicative of glycolysis inhibition. This metabolic shift profoundly affected immune cell function, resulting in impaired T cell proliferation and reduced cytokine secretion. These findings highlight the critical role of glucose metabolism in T cell activation and underscore the therapeutic potential of targeting metabolic pathways in immunotherapy. Further research examined the effects of BAY-876 on macrophage inflammatory responses, a crucial component of immune regulation. The data revealed that BAY-876 treatment reduced the inflammatory capacity of macrophages, as evidenced by decreased expression of pro-inflammatory cytokines and markers. This suggests that targeting GLUT1 with BAY-876 can modulate macrophage function and polarization, providing new insights into the complex interplay between metabolism and immune responses. In conclusion, the presented data provide valuable insights into the effects of the GLUT1 inhibitor BAY-876 on T cells and macrophages. By investigating the impact of metabolic modulation on immune cell function, this research advances our understanding of immune cell biology and paves the way for the development of innovative immunotherapies targeting metabolic pathways. The findings presented herein have significant implications for the field of immunology and offer promising directions for future research in precision medicine approaches within immunotherapy.

Publication Details

Journal
Online Publication Service of Würzburg University (Würzburg University)
Published
2025-01-01
DOI
https://doi.org/10.25972/opus-39359
Primary Topic
Cardiac Fibrosis and Remodeling
Type
article
Field-Weighted Citation Impact
0.00
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article

Characterization of the effect of a GLUT1 inhibitor on macrophages and T cells for modulating the immune response to myocardial infarction

Online Publication Service of Würzburg University (Würzburg University)
Cardiac Fibrosis and Remodeling
article

Characterization of the effect of a GLUT1 inhibitor on macrophages and T cells for modulating the immune response to myocardial infarction

article en

Abstract

The intricate relationship between glucose metabolism and immune cell function, with a specific focus on the role of the glucose transporter-1 (GLUT1), is crucial in modulating T cells and macrophages. Through a series of extensive in vitro experiments, this work aims to elucidate the effects of BAY-876, the specific GLUT1 inhibitor, on these immune cell populations and assess its potential as a therapeutic agent in immune modulation. The here presented study utilized primary T cells and macrophages to explore the impact of BAY-876 on key immune cell functions. The results demonstrated that BAY- 876 treatment led to a significant reduction in glucose uptake and lactate production in T cells, indicative of glycolysis inhibition. This metabolic shift profoundly affected immune cell function, resulting in impaired T cell proliferation and reduced cytokine secretion. These findings highlight the critical role of glucose metabolism in T cell activation and underscore the therapeutic potential of targeting metabolic pathways in immunotherapy. Further research examined the effects of BAY-876 on macrophage inflammatory responses, a crucial component of immune regulation. The data revealed that BAY-876 treatment reduced the inflammatory capacity of macrophages, as evidenced by decreased expression of pro-inflammatory cytokines and markers. This suggests that targeting GLUT1 with BAY-876 can modulate macrophage function and polarization, providing new insights into the complex interplay between metabolism and immune responses. In conclusion, the presented data provide valuable insights into the effects of the GLUT1 inhibitor BAY-876 on T cells and macrophages. By investigating the impact of metabolic modulation on immune cell function, this research advances our understanding of immune cell biology and paves the way for the development of innovative immunotherapies targeting metabolic pathways. The findings presented herein have significant implications for the field of immunology and offer promising directions for future research in precision medicine approaches within immunotherapy.

Online Publication Service of Würzburg University (Würzburg University)
Openalex Percentile: Top 38%
Cardiac Fibrosis and Remodeling
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