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Epigenetic programming underpins B cell dysfunction in human SLE.

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Systemic lupus erythematosus (SLE) involves pathogenic B cells. This study reveals early epigenetic changes in naive B cells, driven by transcription factors AP-1, EGR, and T-BET, leading to B cell dysfunction in SLE.

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Area of Science:

  • Immunology
  • Epigenetics
  • Molecular Biology

Background:

  • Systemic lupus erythematosus (SLE) is an autoimmune disease marked by pathogenic B cell expansion.
  • The epigenetic underpinnings of B cell subsets in SLE are not fully understood.

Purpose of the Study:

  • To investigate the epigenetic architecture and transcriptional profiles of human B cell subsets in SLE patients.
  • To identify molecular differences contributing to pathogenic B cell dysfunction.

Main Methods:

  • Analysis of DNA methylomes, chromatin accessibility, and transcriptomes from five human B cell subsets.
  • Comparison between B cells from SLE patients and healthy controls.

Main Results:

  • Defined a differentiation hierarchy for B cell subsets and elucidated epigenetic/transcriptional differences between effector and memory B cells.
  • Identified an early SLE molecular signature in naive B cells, characterized by accessible chromatin enriched for AP-1 and EGR transcription factor motifs.
  • Demonstrated synergistic action of AP-1, EGR, and T-BET in shaping the epigenome of expanded SLE effector B cells.

Conclusions:

  • Established the molecular foundation for pathogenic B cell dysfunction in SLE.
  • Highlighted the role of early epigenetic alterations in naive B cells in SLE pathogenesis.