Prof. Marc Scherlinger
Marc Scherlinger is a Professor of Rheumatology at Strasbourg University Hospitals, France. His main research interests include clinical and translational research in systemic autoimmune diseases, particularly systemic lupus erythematosus, with a focus on B-cell-targeted therapies, immune dysregulation, and thromboinflammation. He is actively involved in international research collaborations and initiatives aimed at advancing innovative therapies for severe autoimmune diseases.
| Oral 0877| Sunday, 08.11.26 09:45 Abstracts: Systemic Lupus Erythematosus – Treatment: Clinical TrialsPresenting author: Q. Hu (China) Title: Subcutaneous RXIM002, a Targeted Lipid Nanoparticle Circular RNA Therapy, for In Vivo Anti-CD19 CAR T-Cell Generation in Refractory SLE  This first-in-human study evaluated subcutaneous RXIM002, a targeted lipid nanoparticle delivering circular RNA to generate anti-CD19 CAR T cells in vivo, in six patients with refractory SLE. CAR T cells were detectable within 24 hours and persisted for up to 60 days, predominantly in effector memory T-cell subsets. All patients achieved substantial B-cell depletion and clinical improvement (mean SLEDAI-2K reduction of 8.3 points), with only grade 1 CRS and no ICANS or infections reported. These preliminary findings provide proof of concept for a non-viral, subcutaneous CAR T-cell approach, potentially simplifying access to cellular immunotherapies. |
| Oral 0092| Sunday, 08.11.26 13:30 Abstracts: Systemic Lupus Erythematosus – Diagnosis, Manifestations & Outcomes: SLE General Care Presenting author: J. Vasques-Landim (Brazil) Title: Coronary Artery Calcification is Common Among Systemic Lupus Erythematosus Patients Classified as Low Cardiovascular Risk by the ACC/AHA PREVENT™ Calculator This cross-sectional study investigated the performance of the ACC/AHA PREVENT™ cardiovascular risk calculator in 83 women with systemic lupus erythematosus (SLE) aged 40–60 years. Coronary artery calcification (CAC) was detected in 25.3% of patients. Notably, 57.1% of patients with detectable CAC were categorized as low risk by PREVENT™. The calculator showed limited discrimination for CAC (AUC 0.67), whereas a model incorporating age, serum albumin and the SLICC/ACR Damage Index achieved an AUC of 0.78. These findings highlight the limitations of conventional cardiovascular risk assessment in SLE and suggest that disease-specific factors may improve the identification of subclinical coronary atherosclerosis |
| Oral 0932| Sunday, 08.11.26 15:00 Abstracts: Antiphospholipid Syndrome Presenting author: A. Luta (USA) Title: Clinical and Laboratory Predictors of Recurrent Thrombosis in Patients with Thrombotic Antiphospholipid Syndrome (APS): A Prospective Analysis of the APS ACTION Registry This prospective international study investigated predictors of recurrent thrombosis in 732 patients with thrombotic APS from the APS ACTION Registry. Over a mean follow-up of 5.7 years, 82 patients (11%) experienced recurrent thrombosis. A history of microvascular disease was the only significant independent predictor of recurrence (HR 2.16, 95% CI 1.12–4.15), while elevated anti-β2GPI IgG levels showed a non-significant association. These findings identify microvascular involvement as an important factor for thrombotic risk stratification in APS, although the predictive model showed only modest discrimination. |
| Oral 1848| Monday, 09.11.26 09:00 Abstracts: Reproductive Issues in Rheumatic Disorders Presenting author: M. Hagen (Germany) Title: Pregnancies in Patients with Autoimmune Disease Receiving CAR T-Cell Therapy This international case series reported 14 pregnancies in 13 women previously treated with CD19 CAR T-cell therapy for autoimmune diseases, including eight with SLE. The report describes seven women who delivered, eight neonates assessed, six ongoing pregnancies and one elective termination. No disease flares occurred during pregnancy. Neonatal B-cell counts and immunoglobulin levels were normal, and no CAR T cells were detected. These preliminary findings are reassuring, but larger studies and longer follow-up are needed. |
| Oral 1823| Monday, 09.11.26 10:45 Plenary Session: Plenary II Presenting author: R. A. Furie (USA) Title: Obinutuzumab Induces Histologic Remission and Deep Kidney Parenchymal B-cell Depletion in Patients With Lupus Nephritis: Exploratory Analyses From a Phase III Trial This exploratory analysis of the phase III REGENCY trial evaluated 64 repeat kidney biopsies in patients with lupus nephritis treated with obinutuzumab or placebo. Obinutuzumab significantly increased histological remission and induced profound depletion of kidney-infiltrating B cells. Remarkably, among patients without complete clinical renal response, 52.6% achieved histological remission with obinutuzumab versus 8.3% with placebo. These findings provide evidence of deep tissue B-cell depletion with anti-CD20 therapy and highlight the discrepancy between clinical and histological responses in lupus nephritis. |
| Oral 1862| Monday 09.11.26 13:00 Abstract Session: Rheumatoid Arthritis – Treatment II: Phenotyping and Personalization Presenting author: I. Parodis (Sweden) Title: Post-Treatment Proteinuria Imperfectly Predicts Histological Remission in Lupus Nephritis: Repeat Biopsy Data from ReBioLup Support Reappraisal of Trial Endpoints This prospective multicentre ReBioLup analysis assessed 47 month-12 repeat kidney biopsies. Eight of 47 patients (17%) had proteinuria below 0.5 g/g despite significant renal inflammation (NIH activity index ≥4), while 5/47 (11%) had proteinuria above 1 g/g with minimal or no histological activity. The optimal proteinuria threshold for histological remission was 0.22 g/g (AUC 0.79). These findings demonstrate discordance between proteinuria and tissue activity and support reconsideration of proteinuria-based trial endpoints. |
| Oral 2839| Tuesday, 10.11.26 08:00 Abstracts: Systemic Lupus Erythematosus – Diagnosis, Manifestations & Outcomes III: SLE Future Directions Presenting author: E. Morand (Australia) Title: A New Endpoint for SLE Clinical Trials: The Treatment Response Measure for Systemic Lupus Erythematosus Clinical Trials (TRM-SLE) This international consensus initiative developed TRM-SLE, a novel, patient-centred treatment response measure for SLE clinical trials. Involving 125 clinicians, 27 patient representatives and 46 other experts, the framework defines clinically meaningful improvement across eight disease domains, including arthritis, skin manifestations, nephritis and serositis. Overall response is classified as TRM-100 (improvement in all active domains) or TRM-1 (improvement in at least one domain). This new endpoint aims to overcome limitations of existing composite measures, although validation in clinical trial datasets is ongoing. |