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O19 Evolution of kidney antibody secreting cells molecular signature in lupus patients with active nephritis upon immunosuppressive therapy
  1. Etienne Crickx1,2,
  2. Farah Tamirou3,
  3. Tessa Huscenot1,4,
  4. Nathalie Costedoat5,
  5. Marion Rabant6,
  6. Alexandre Karras7,
  7. Tatiana Fadeev1,
  8. Véronique Le Guern5,
  9. Philippe Remy8,
  10. Aurélie Hummel9,
  11. Bernard Lauwerys3,
  12. Jean-Claude Weill1,
  13. Claude-Agnès Reynaud1,
  14. Frédéric Houssiau3 and
  15. Matthieu Mahévas1,2
  1. 1Institut Necker-Enfants-Malades, INSERM-U1151/CNRS-UMS 8253, Université Paris Descartes, Paris
  2. 2APHP, Internal Medicine Dept., Henri-Mondor Hospital, Université Paris-Est, Créteil, France
  3. 3Service de Rhumatologie, Cliniques Universitaires Saint-Luc, Brussels, Belgium
  4. 4APHP, Dept. of Internal Medicine, Lariboisière Hospital, Paris
  5. 5APHP, Internal Medicine Dept., Cochin Hospital, Paris
  6. 6APHP, Pathology Dept., Necker Hospital, Paris
  7. 7APHP, Nephrology Dept., HEGP, Paris
  8. 8APHP, Nephrology Dept., Henri-Mondor Hospital, Créteil
  9. 9APHP, Nephrology Dept., Necker Hospital, Paris, France


Background/Purpose Pathogenic antibody-secreting cells (ASC) are poorly characterized in human lupus nephritis (LN). Our objective was to compare the single cell molecular signature of ASC in kidney and urine from patients with active LN, either untreated or after immunosuppressive therapy failure.

Methods ASC were identified by anti-CD138 staining on fixed renal biopsies from patients with active LN. We sorted single-ASC from fresh renal biopsies to perform gene expression profiling. ASC transcriptional program from urine of untreated LN patients was assessed at diagnosis and after a prospective follow up during induction therapy.

Results Interstitial infiltrates of CD138+ ASC were found in untreated (N=15) and refractory patients (N=6). Single cell molecular signature of kidney ASC from untreated patients revealed that these cells were mostly plasmablasts and contrasted with ASC signature from patients with mycophenolate mofetil failure that expressed long-lived plasma cells genes and clustered with long-lived bone marrow ASC from healthy donors. A plasmablast signature was observed in urine ASC at diagnosis, similar to their kidney counterpart. The concentration of urine ASC from 22 untreated patients correlated with ISN/RPS classification, with higher concentration in class IV patients (p<0.01).

Conclusion These results suggest that plasmablasts infiltrate kidney of untreated LN patients, while kidney long-lived ASC may contribute to the failure of immunosuppressive therapy.

Acknowledgement This work was funded by FOREUM.

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