RT Journal Article SR Electronic T1 O19 Evolution of kidney antibody secreting cells molecular signature in lupus patients with active nephritis upon immunosuppressive therapy JF Lupus Science & Medicine JO Lupus Sci Med FD Lupus Foundation of America SP A16 OP A17 DO 10.1136/lupus-2020-eurolupus.30 VO 7 IS Suppl 1 A1 Crickx, Etienne A1 Tamirou, Farah A1 Huscenot, Tessa A1 Costedoat, Nathalie A1 Rabant, Marion A1 Karras, Alexandre A1 Fadeev, Tatiana A1 Guern, Véronique Le A1 Remy, Philippe A1 Hummel, Aurélie A1 Lauwerys, Bernard A1 Weill, Jean-Claude A1 Reynaud, Claude-Agnès A1 Houssiau, Frédéric A1 Mahévas, Matthieu YR 2020 UL http://lupus.bmj.com/content/7/Suppl_1/A16.3.abstract AB 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.