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Updated: Jan 7, 2026

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Altered B cell metabolic pathways characterize type 1 diabetes progression.

Holly Conway1,2, Jessica Bernard1,2, Rachel Ramos1,2

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Journal of Immunology (Baltimore, Md. : 1950)
|December 27, 2025
PubMed
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Regulatory B cells (Bregs) are crucial for preventing type 1 diabetes (T1D). In this study, NOD mice B cells showed altered metabolism and reduced HIF-1α, impacting IL-10 production and immune tolerance.

Keywords:
B cellhypoxiaimmunometabolismtype 1 diabetes

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Area of Science:

  • Immunology
  • Metabolic pathways
  • Autoimmune diseases

Background:

  • Type 1 diabetes (T1D) involves immune-mediated destruction of pancreatic beta cells, with B cells playing a dual role as antigen presenters and regulators.
  • Regulatory B cells (Bregs) producing IL-10 are protective in autoimmunity, but their function is impaired in T1D.
  • Hypoxia-inducible factor 1α (HIF-1α) signaling promotes Breg expansion via glycolysis, yet its role in T1D B cells is unclear.

Purpose of the Study:

  • To investigate the interplay between B cell differentiation, metabolism, and HIF-1α signaling in autoimmune diabetes.
  • To determine if impaired Breg function in T1D is due to intrinsic B cell defects or microenvironmental factors.
  • To elucidate the mechanisms of B cell-mediated suppression of pathogenic T cells in diabetes.

Main Methods:

  • Comparative analysis of B cell metabolism and function between non-obese diabetic (NOD) mice and non-autoimmune B6 mice.
  • Assessment of glucose uptake, IL-10 expression, and HIF-1α signaling pathways in B cells.
  • Evaluation of HIF-1α-dependent gene induction and glycolytic flux.

Main Results:

  • B cells from NOD mice exhibit increased glucose uptake and IL-10 production compared to B6 mice.
  • Despite elevated IL-10, NOD B cells show reduced HIF-1α levels and attenuated HIF-1α-dependent gene expression.
  • These findings suggest HIF-1α has a diminished role in regulating IL-10 production in NOD B cells, and IL-10 alone is insufficient for immune tolerance.

Conclusions:

  • B cell metabolism is dynamically remodeled during autoimmune diabetes progression.
  • Genetic and microenvironmental factors reprogram B cell metabolism and function in T1D.
  • Therapeutic strategies for T1D should consider IL-10 independent pathways and B cell-extrinsic mechanisms for immune modulation.