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Age-related changes in B cell metabolism.

Raj K Kurupati1, Larissa H Haut1, Kenneth E Schmader2

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Aging impairs B cell metabolism, weakening antibody responses to vaccines. This study reveals metabolic defects in aged B cells, including mitochondrial dysfunction and impaired one-carbon metabolism, contributing to reduced vaccine efficacy in the elderly.

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B cell metabolismantibody responsesvaccination

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Area of Science:

  • Immunology
  • Cellular Metabolism
  • Aging Research

Background:

  • Antibody production by B cells is crucial for vaccine efficacy.
  • Immune responses, including antibody production, are known to decline with age.
  • The underlying cellular mechanisms contributing to age-related immune decline require further elucidation.

Purpose of the Study:

  • To investigate the role of metabolic changes in B cells contributing to the attenuated antibody responses observed in aged humans following influenza vaccination.

Main Methods:

  • Analysis of B cell mitochondrial function, including reactive oxygen species (MROS) and mitochondrial mass (MM).
  • Assessment of metabolic pathways such as glycolysis and oxidative phosphorylation using Seahorse analysis.
  • Transcriptome analysis to identify defects in metabolic pathways, including one-carbon metabolism.

Main Results:

  • Aging altered mitochondrial function in B cells, increasing MROS and MM in some subsets while decreasing expression of SIRT1, FOXO1, and CPT-1.
  • Aged B cells exhibited minor defects in glycolysis but significant reductions in oxidative phosphorylation post-activation.
  • Transcriptome analysis revealed pronounced defects in one-carbon metabolism, essential for amino acid and nucleotide synthesis.

Conclusions:

  • Metabolic alterations, particularly mitochondrial dysfunction and impaired one-carbon metabolism, are evident in aged B cells.
  • The reduced capacity of aged B cells to enhance their metabolism upon activation contributes to weakened antibody responses in the elderly.
  • These findings highlight metabolic reprogramming as a key factor in age-related immunosenescence and reduced vaccine effectiveness.