General Assembly 2026 — key decisions and next steps

Our Lupus Center is dedicated to clinical care of lupus patients and to translational and clinical research, with a strong cross-fertilization approach. Clinical care is provided by two full-time rheumatologists (Frédéric Houssiau and Farah Tamirou), a dedicated nurse coordinator (Séverine Nieuwland-Husson) and 4 rheumatology trainees. Every week, we run two Lupus Clinics, allowing us to see 40-50 lupus patients/week, half of them with lupus nephritis. We have access to our own in-patient beds for acute cases. Our Lupus Center is part of the European Reference Network ReCONNET (Connective tissue and Musculoskeletal Diseases). More than 600 lupus patients are registered in our electronic data base.

Lupus nephritis is our main clinical research topic, with more than 50 publications in this specific field dealing with the diagnosis, prognosis and treatment of renal involvement. Our group designed and run two European investigator-initiated trials which helped to define the optimal therapy of lupus nephritis. We recently defined the early proteinuria target which predicted long-term renal outcome. We have started an ambitious renal re-biopsy program Click Here

Selected recent publications

Per-protocol repeat kidney biopsy portends relapse and long-term outcome in incident cases of proliferative lupus nephritis. Parodis et al. Rheumatology (Oxford) 2020; 59: 3424-34.
Disease severity of proliferative lupus nephritis in Maghrebians. Tamirou et al. Lupus 2018 ; 27 : 1387-92.
A proteinuria cut-off level of 0.7 g/day after 12 months of treatment best predicts long-term renal outcome in lupus nephritis : data from the MAINTAIN Nephritis Trial. Tamirou et al. Lupus Sci Med 2015 ; 2 : e000123.
Prediction of prognosis and renal outcome in lupus nephritis. Parodis et al. Lupus Sci Med 2020 ; 7 : e000389.
Intrarenal activation of adaptive immune effectors is associated with tubular damage and impaired renal function in lupus nephritis. Pamfil C. et al. Ann Rheum Dis 2018. doi: 10.1136/annrheumdis-2018-213485.
Time to change the primary outcome of lupus trials. Houssiau FA. Ann Rheum Dis 2018. doi:10.1136/annrheumdis-2018-213788.
Ustekinumab: a promising drug for SLE? Costedoat-Chalumeau N and Houssiau FA. Lancet 2018. doi:10.1016/S0140-6736(18)32330-4.
Brief Report: The Euro-Lupus low-dose intravenous cyclophosphamide regimen does not impact the ovarian reserve, as measured by serum levels of anti-Müllerian hormone. Tamirou F et al. Arthritis Rheumatol 2017;69: 1267.
Long-term follow-up of the MAINTAIN Nephritis Trial, comparing azathioprine and mycophenolate mofetil as maintenance therapy of lupus nephritis. Tamirou F et al. Ann Rheum Dis 2016; 75: 526-31.
Contacts
Cliniques universitaires Saint-Luc
10 Avenue Hippocrate 10, B 1200 Woluwe-Saint-Lambert, Bruxelles Belgium
Phone: 02 764 11 11
Fax: 02 764 37 03

Languages:
English or French speaking.

Recommended period: to be defined with the awardees

CHUC Lupus Clinic (Coimbra)

The Lupus Clinic at the Centre for Rheumatology, University College (London)

Centre de Référence Maladies Rares – Hôpital Cochin (Paris)

UIC – Unidade de Imunologia Clínica – Hospital de Santo António (Porto)

Karolinska University Hospital (Stockholm)

Rheumatology Unit, Department of Medicine, University of Padua (Padua)

Department of Autoimmune Diseases of the Hospital Clínic de Barcelona (Barcelona)

Centre Hospitalier Universitaire (CHU) de Bordeaux (Bordeaux)

Department of Rheumatology, Clinical Immunology and Allergy, University Hospital of Iraklio and University of Crete Medical School (Iraklio)

Center for Genomics and Oncological Research (GENyO) – Complex Diseases Group (Granada)

University of Leeds (Leeds)

Rheumatology and Clinical Immunology Unit ASST-Spedali Civili and University of Brescia (Brescia)

University of Birmingham and Sandwell and West Birmingham NHS Trust (Birmingham City Hospital)

Leiden University Medical Center

SLEuro Centers

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A high burden of SLE risk genes is associated with persistent activation of the interferon system in patients with lupus.

Comment on: Single-cell RNA-seq reveals a persistent interferon signature in immune cells from  systemic lupus erythematosus patients with high versus low polygenic risk scores despite antimalarial  treatment. J Autoimmun. 2026 May 12:161:103575. doi: 10.1016.  Commented by: Lars Rönnblom, Department of Medical Sciences, Uppsala University, Sweden.    Genome-wide association studies have identified more than 300 loci associated to increased risk for  SLE. For the majority of the gene variants in these loci the functional consequences in the SLE disease  process are unknown. However, a large proportion of identified risk genes are connected to the  interferon signaling pathway and contribute to the interferon signature in SLE. Calculating a polygenic  risk score (PRS) is a method to quantify the cumulative genetic burden in a single patient and studies  have shown that patients with a high PRS have a more severe disease phenotype with increased  organ damage and reduced survival, compared to individuals with a low PRS.   Antimalarial therapy is a well-established treatment of SLE and have shown efficacy in a large  proportion of patients. The therapeutic effect is partly mediated by down regulation of the activated  interferon system, which is connected to clinical response. However, despite therapeutic  concentrations of hydroxychloroquine, many patients still have flares and accumulation of organ  damage. The main objective of the present study was therefore to clarify if antimalarial treatment has  different effects in patients with a high or a low PRS.  SLE patients in remission with a high or a low PRS were compared in gene expression profile at single  cell level on peripheral blood mononuclear cells. A total of 6 healthy controls and 16 matched  patients treated with similar antimalarial doses, but no corticosteroids, were investigated. On  average, 9636 cells were analyzed from each donor and 2724 genes detected per cell. Despite similar  clinical picture, patients with a high PRS had a prominent interferon signature across multiple  immune cell types, compared to patients with a low PRS who had a weak expression of interferon  stimulated genes only in monocytes. Pathway analysis revealed that the interferon signaling pathway 

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