CD24(hi)CD27⁺ and plasmablast-like regulatory B cells in human chronic graft-versus-host disease

Blood. 2015 Mar 12;125(11):1830-9. doi: 10.1182/blood-2014-09-599159. Epub 2015 Jan 20.

Abstract

Interleukin 10 (IL-10)-producing B cells (regulatory B cells [Bregs]) regulate autoimmunity in mice and humans, and a regulatory role of IL-10-producing plasma cells has been described in mice. Dysfunction of B cells that maintain homeostasis may play a role in the pathogenesis of chronic graft-versus-host disease (cGVHD) after allogeneic stem cell transplantation. Here, we found a relation between decreased Breg frequencies and cGVHD severity. An impaired ability of B cells to produce IL-10, possibly linked to poor signal transducer and activator of transcription 3 and extracellular signal-regulated kinase phosphorylation, was found in patients with active cGVHD. IL-10 production was not confined to a single B-cell subset, but enriched in both the CD24(hi)CD27(+) and CD27(hi)CD38(hi) plasmablast B-cell compartments. In vitro plasmablast differentiation increased the frequency of IL-10-producing B cells. We confirmed that allogeneic transplant recipients had an impaired reconstitution of the memory B-cell pool. cGVHD patients had less CD24(hi)CD27(+) B cells and IL-10-producing CD24(hi)CD27(+) B cells. Patients with cGVHD had increased plasmablast frequencies but decreased IL-10-producing plasmablasts. These results suggest a role of CD24(hi)CD27(+) B-cell and plasmablast-derived IL-10 in the regulation of human cGVHD.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • ADP-ribosyl Cyclase 1 / metabolism
  • Adult
  • Aged
  • Animals
  • B-Lymphocytes, Regulatory / immunology*
  • B-Lymphocytes, Regulatory / metabolism
  • B-Lymphocytes, Regulatory / pathology
  • CD24 Antigen / metabolism*
  • Cell Differentiation
  • Chronic Disease
  • Female
  • Graft vs Host Disease / etiology
  • Graft vs Host Disease / immunology*
  • Graft vs Host Disease / pathology
  • Hematopoietic Stem Cell Transplantation / adverse effects
  • Humans
  • Interleukin-10 / biosynthesis
  • MAP Kinase Signaling System
  • Male
  • Membrane Glycoproteins / metabolism
  • Mice
  • Middle Aged
  • Plasma Cells / immunology
  • Plasma Cells / metabolism
  • Plasma Cells / pathology
  • Prospective Studies
  • STAT3 Transcription Factor / metabolism
  • Signal Transduction
  • Tumor Necrosis Factor Receptor Superfamily, Member 7 / metabolism*
  • Young Adult

Substances

  • CD24 Antigen
  • CD24 protein, human
  • IL10 protein, human
  • Membrane Glycoproteins
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Tumor Necrosis Factor Receptor Superfamily, Member 7
  • Interleukin-10
  • CD38 protein, human
  • ADP-ribosyl Cyclase 1