Welcome to the 2021 LUPUS CORA Meeting Program Scheduling

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Displaying One Session

LUPUS Topics || ASC03 BIOMARKERS IN SLE, LUPUS Topics || ASC05 DISEASE ACTIVITY AND DISEASE FLARES, No Topic Needed

Session Type
Parallel Session (Lupus)
Date
Wed, 06.10.2021
Session Time
14:00 - 16:00
Room
Hall 1
Chair(s)
  • Lindsey Criswell (United States of America)
  • Carlo Chizzolini (Switzerland)

BAFF in systemic lupus erythematosus.

Presenter
  • Carlo Chizzolini (Switzerland)
Lecture Time
14:00 - 14:15

Live Q&A

Lecture Time
14:15 - 14:30

New insights into the role of B lineage cells in SLE

Presenter
  • Thomas Dörner (Germany)
Lecture Time
14:30 - 14:45

Live Q&A

Lecture Time
14:45 - 15:00

What we are learning from single cell analyses of renal myeloid cells in lupus nephritis – from mouse to human

Presenter
  • Anne Davidson (United States of America)
Lecture Time
15:00 - 15:15

Live Q&A

Lecture Time
15:15 - 15:30

GENE SIGNATURE FINGERPRINTS DIVIDE SLE PATIENTS IN SUBGROUPS WITH SIMILAR BIOLOGICAL DISEASE PROFILES: A MULTICENTER LONGITUDINAL STUDY

Presenter
  • Javad Wahadat (Netherlands)
Lecture Time
15:30 - 15:36

Abstract

Background and Aims

Clinical phenotyping and predicting treatment responses in Systemic Lupus Erythematosus (SLE) patients is challenging. Extensive blood transcriptional profiling has identified various gene modules that seem promising for stratification of SLE patients. This study was undertaken to translate transcriptomic data into gene signatures suitable for introduction into clinical practice and to associate these signatures with disease activity.

Methods

RT-PCR of multiple genes from the Interferon M1.2, Interferon M5.12, neutrophil (NPh)- and plasma cell (PLC) modules followed by a principle component analysis was used to identify indicator genes per gene signature. Gene signatures were measured in longitudinal samples from two childhood onset SLE cohorts (n=101 and n=34, respectively) and associated with clinical features. Disease activity was measured using SELENA-SLEDAI. Cluster analysis subdivided patients into three fingerprint groups termed 1) all-signatures-low, 2) only IFN high (M1.2 and/or M5.12) and 3) high NPh and/or PLC.

Results

All gene signatures were significantly associated with disease activity in cross-sectionally collected samples. The PLC signature showed the highest association with disease activity. Also, in longitudinally collected samples, the PLC signature was associated with disease activity and showed a decrease over time. When patients were divided into fingerprints, the highest disease activity was observed in the high NPh and/or PLC group. The lowest disease activity was observed in the all-signatures-low group. The same distribution could be reproduced in samples from an independent SLE cohort.

Conclusions

Gene signatures are associated with disease activity and can be suitable tools to sub-classify SLE patients into groups with similar pathogenically activated immunological pathways.

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Live Q&A

Lecture Time
15:36 - 15:40

ASSOCIATIONS BETWEEN EARLY CHANGES IN CIRCULATING B CELL SUBSETS AND SEVERE FLARE IN SYSTEMIC LUPUS ERYTHEMATOSUS – RESULTS FROM THREE PHASE III TRIALS OF BELIMUMAB

Presenter
  • Ioannis Parodis (Sweden)
Lecture Time
15:40 - 15:46

Abstract

Background and Aims

We aimed to investigate early changes in B cell subsets in relation to flare during standard therapy plus belimumab or placebo within the frame of three phase III clinical trials of belimumab in SLE.

Methods

We analyzed pooled 52-week data from BLISS-76 (N=819), BLISS-SC (N=836), and BLISS North-East Asia (N=60). B cell subsets were determined with flow-cytometry. Severe flares were evaluated according to the SELENA-SLEDAI Flare Index. We investigated B cell changes relative to baseline using proportional hazards regression.

Results

Decreases in CD19+CD20-CD138+ long-lived (HR: 0.7; 95% CI: 0.56–0.98; P=0.034) and CD19+CD38brightCD27bright SLE-associated plasma cells (HR: 0.7; 95% CI: 0.50–0.87; P=0.003) from baseline through week 24 were negatively associated with the development of severe flare through week 52, and decreases in naïve CD19+CD20+CD27- B cells showed a similar trend (HR: 0.7; 95% CI: 0.56–1.00; P=0.051). No such association was observed for early changes in CD19+CD20+CD27+ memory B cells, CD19+CD20+CD69+ activated B cells or CD19+CD20-CD27bright short-lived plasma cells. The association with CD19+CD38brightCD27bright SLE-associated plasma cells held true for patients treated with belimumab (HR: 0.7; 95% CI: 0.47–0.97; P=0.032) but not placebo, while placebo receivers showing reductions in CD19+CD20-CD138+ long-lived plasma cells displayed lower probability to flare (HR: 0.6; 95% CI: 0.38–0.87; P=0.009).

Conclusions

Early decreases in long-lived circulating plasma cells were negatively associated with severe flares in patients with active SLE treated with standard immunosuppression with or without add-on belimumab, while reductions in circulating CD19+CD38brightCD27bright plasma cells may prove a useful early marker of favorable response to belimumab therapy.

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Live Q&A

Lecture Time
15:46 - 15:50

Closing Remarks

Lecture Time
15:50 - 16:00