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Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Secreted high mobility group box protein 1 (HMGB1) influences adaptive immunity and cellular stress responses.
  • The specific function of HMGB1 within B cells has remained largely unexplored.

Purpose of the Study:

  • To investigate the role of HMGB1 in peripheral B cell homeostasis and humoral immunity.
  • To elucidate the molecular mechanisms by which HMGB1 regulates B cell receptor (BCR) signaling and function.

Main Methods:

  • Conditional deletion of the Hmgb1 gene in B cells.
  • Analysis of B cell populations, including marginal zone B cells and B1a cells.
  • Assessment of antigen-specific antibody responses.
  • Investigation of BCR signaling pathways, CD21 expression, and lymphoid enhancer-binding factor 1 (LEF1) levels.
  • Examination of actin reorganization and the MST1/DOCK8/WASP signaling axis.

Main Results:

  • Conditional deletion of HMGB1 in B cells resulted in expanded marginal zone B cells and reduced B1a cells.
  • B cell-specific Hmgb1 deletion led to impaired antigen-specific antibody responses.
  • HMGB1 deficiency enhanced proximal and distal BCR signaling, likely due to increased CD21 expression, lowering the BCR activation threshold.
  • HMGB1 loss correlated with reduced LEF1 levels and increased CD21 transcription, as HMGB1 binds the Lef1 promoter.
  • HMGB1 constrained actin reorganization by suppressing the MST1/DOCK8/WASP pathway, impacting BCR clustering and signalosome recruitment.

Conclusions:

  • HMGB1 is essential for maintaining peripheral B cell homeostasis and effective humoral immunity.
  • HMGB1 acts as a dual regulator, controlling B cell activation thresholds both transcriptionally (via LEF1/CD21) and cytoskeletally (via actin dynamics).
  • These findings highlight HMGB1's critical role in optimizing BCR signaling and B cell function.