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Interleukin-10-producing plasmablasts exert regulatory function in autoimmune inflammation.

Masanori Matsumoto1, Akemi Baba2, Takafumi Yokota3

  • 1Laboratory for Lymphocyte Differentiation, WPI Immunology Frontier Research Center, Osaka University, Suita, Osaka 565-0871, Japan; Laboratory for Lymphocyte Differentiation, RIKEN Center for Integrative Medical Sciences (IMS), Yokohama, Kanagawa 230-0045, Japan.

Immunity
|December 9, 2014
PubMed
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Regulatory B cells, specifically plasmablasts in lymph nodes, secrete interleukin-10 (IL-10) to suppress autoimmune diseases like experimental autoimmune encephalomyelitis (EAE). These findings highlight plasmablasts as crucial IL-10 producers in controlling inflammation.

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Area of Science:

  • Immunology
  • Autoimmunity
  • Cell Biology

Background:

  • B cells are known to suppress autoimmunity through interleukin-10 (IL-10) secretion.
  • The specific B cell subsets responsible for IL-10 production and in vivo regulatory function remain unidentified.

Purpose of the Study:

  • To identify the in vivo IL-10-producing B cells with regulatory function during experimental autoimmune encephalomyelitis (EAE).
  • To elucidate the role of these regulatory B cells in controlling autoimmune inflammation.

Main Methods:

  • Utilized IL-10 reporter mice to track IL-10 expression in B cells during EAE.
  • Genetically ablated key transcription factors (Blimp1, IRF4) in B lineage cells to assess the impact on EAE and plasmablast function.
  • Investigated the regulatory mechanisms involving IL-10 and dendritic cell function.

Main Results:

  • Plasmablasts in draining lymph nodes (dLNs), not splenic B cells, were the predominant IL-10 producers during EAE.
  • These IL-10-producing plasmablasts were specifically generated during EAE inflammation.
  • Genetic ablation of plasmablasts led to exacerbated EAE, indicating their protective role.
  • IRF4 was identified as a positive regulator of IL-10 production, which inhibits dendritic cell activity and pathogenic T cell generation.

Conclusions:

  • Plasmablasts in dLNs are key IL-10-producing regulatory B cells that limit autoimmune inflammation.
  • The study emphasizes the critical role of plasmablasts in immune regulation during autoimmune conditions.
  • IRF4-mediated IL-10 production by plasmablasts is a crucial mechanism for suppressing EAE development.