Bierling T, Gumann A, Ottmann S, Schulz S, Weckwerth L, Thomas J, Geßner A, Wichert M, Kuwert F, Rost F, Hauke M, Freudenreich T, Mielenz D, Jäck HM, Pracht K (2024)
Publication Language: English
Publication Type: Journal article
Publication year: 2024
Book Volume: 43
Article Number: 113739
Journal Issue: 2
DOI: 10.1016/j.celrep.2024.113739
Glucose uptake increases during B cell activation and antibody-secreting cell (ASC) differentiation, but conflicting findings prevent a clear metabolic profile at different stages of B cell activation. Deletion of the glucose transporter type 1 (GLUT1) gene in mature B cells (GLUT1-cKO) results in normal B cell development, but it reduces germinal center B cells and ASCs. GLUT1-cKO mice show decreased antigen-specific antibody titers after vaccination. In vitro, GLUT1-deficient B cells show impaired activation, whereas established plasmablasts abolish glycolysis, relying on mitochondrial activity and fatty acids. Transcriptomics and metabolomics reveal an altered anaplerotic balance in GLUT1-deficient ASCs. Despite attempts to compensate for glucose deprivation by increasing mitochondrial mass and gene expression associated with glycolysis, the tricarboxylic acid cycle, and hexosamine synthesis, GLUT1-deficient ASCs lack the metabolites for energy production and mitochondrial respiration, limiting protein synthesis. We identify GLUT1 as a critical metabolic player defining the germinal center response and humoral immunity.
APA:
Bierling, T., Gumann, A., Ottmann, S., Schulz, S., Weckwerth, L., Thomas, J.,... Pracht, K. (2024). GLUT1-mediated glucose import in B cells is critical for anaplerotic balance and humoral immunity. Cell Reports, 43(2). https://doi.org/10.1016/j.celrep.2024.113739
MLA:
Bierling, Theresa, et al. "GLUT1-mediated glucose import in B cells is critical for anaplerotic balance and humoral immunity." Cell Reports 43.2 (2024).
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