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Takayasu arteritis is characterised by disturbances of B cell homeostasis and responds to B cell depletion therapy with rituximab
  1. Bimba F Hoyer1,2,
  2. Imtiaz M Mumtaz1,2,
  3. Konstanze Loddenkemper1,
  4. Anne Bruns1,
  5. Claudia Sengler3,
  6. Kay-Geert Hermann4,
  7. Sofiane Maza5,
  8. Rolf Keitzer3,
  9. Gerd-Rüdiger Burmester1,
  10. Frank Buttgereit1,
  11. Andreas Radbruch2,
  12. Falk Hiepe1,2
  1. 1Department of Medicine (Clinic for Rheumatology and Clinical Immunology), Charité-Universitätsmedizin Berlin, Berlin, Germany
  2. 2German Rheumatism Research Center, Berlin-Leibniz Institute, Germany
  3. 3Department of Pediatric Rheumatology, Charité-Universitätsmedizin Berlin, Berlin, Germany
  4. 4Department of Radiology, Charité-Universitätsmedizin Berlin, Berlin, Germany
  5. 5Department of Nuclear Medicine, Charité-Universitätsmedizin Berlin, Berlin, Germany
  1. Correspondence to Falk Hiepe, Department of Medicine, Clinic for Rheumatology and Clinical Immunology, Charité–Universitätsmedizin Berlin and German Rheumatism Research Center Berlin-Leibniz Institute, Charitéplatz 1, D-10117 Berlin, Germany; falk.hiepe{at}charite.de

Abstract

Introduction Takayasu arteritis (TA) is a large vessel vasculitis involving the aorta and its major branches. T cell-mediated autoimmunity is thought to play a major role in its pathogenesis, while the role of B cells is still unclear.

Methods B cell subsets in the peripheral blood of 17 patients with TA were analysed and compared with nine patients with active systemic lupus erythematosus (SLE) and nine healthy controls by flow cytometry. Based on these findings, three patients with active refractory TA were treated with B cell depletion therapy (BCDT) using monoclonal anti-CD20 antibodies (rituximab).

Results The absolute number and frequency of peripheral blood CD19+/CD20/CD27high antibody-secreting cells in patients with active TA was significantly higher than in healthy donors. As in active SLE, the majority of these cells are newly generated plasmablasts which significantly correlated with TA activity. Three patients with active refractory TA and expansion of plasmablasts were successfully treated with BCDT, which resulted in remission.

Conclusion Disturbances of B cell homeostasis may be critical in TA. Circulating plasmablasts could be a useful biomarker of disease activity and a tool for selecting appropriate candidates for BCDT. B cells and plasmablasts/plasma cells may therefore represent novel targets for effective therapies for TA.

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Footnotes

  • Funding This work was supported by the Deutsche Forschungsgemeinschaft (SFB650) and Roche Pharma AG provided financial support for writing the manuscript.

  • Competing interests None.

  • Patient consent Obtained.

  • Ethics approval This study was conducted with the approval of the ethics committee of Charité-Universitätsmedizin Berlin.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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