SINGLE-CELL PROFILING OF SKIN AND SYNOVIAL FIBROBLASTS IDENTIFIES OPPOSING IFN-α/β REGULATION IN PsO-ARTHRALGIA AND PsA
Abstract format and assignment number: Oral presentation, OP0266
Presenting author: A. Khmelevskaia (Switzerland)
Around 30% of people with psoriasis develop psoriatic arthritis, and those with arthralgia are at highest risk, yet we cannot predict who will progress. Single-cell profiling of skin and synovial fibroblasts identified disease-specific subsets, with interferon-α/β signalling downregulated in PsA skin but upregulated in PsA synovium. This opposing skin-to-joint signature suggests an early mechanism of transition and a possible biomarker to catch progression before arthritis appears.
TWO ORGANOID MODELS OF THE MATERNAL-FETAL INTERFACE TO STUDY FAILING TOLERANCE IN SLE
Abstract format and assignment number: Poster, POS1121
Presenting author: W. Dankers (Netherlands)
Up to half of pregnancies in SLE end in complications, but the maternal-fetal interface cannot be studied directly in patients. The authors built two trophoblast organoid models, one for the placental villi and one for the decidua, and both reproduced a tolerogenic immune environment once immune cells were added. These are the first in vitro systems to capture both interfaces, opening a route to study why tolerance fails in lupus pregnancy and to test interventions.
HIGH-RESOLUTION SPATIAL MAPPING OF THE JIA SYNOVIUM UNCOVERS DISEASE-RELEVANT NICHES
Abstract format and assignment number: Oral presentation, OP0189
Presenting author: J. Inamo (Japan)
The synovium drives juvenile idiopathic arthritis, but how its cells are spatially organised has been unclear. High-resolution spatial transcriptomics defined four recurring cellular niches and specific crosstalk, including a NOTCH3 fibroblast-endothelial axis and a CXCL9-CXCR3 macrophage-CD8 T-cell axis. Mapping which cells act together, and where, reveals candidate pathways and therapeutic targets that bulk approaches miss.
MULTI-OMICS ANALYSIS ELUCIDATES THE TRAJECTORY OF PROGRESSION FROM THE ANTIBODY-POSITIVE PHASE TO ESTABLISHED SYSTEMIC SCLEROSIS
Abstract format and assignment number: Oral presentation, OP004
Presenting author: H. Yin (China)
Systemic sclerosis carries high mortality, so recognising it before organ damage occurs is critical. Combining transcriptomics and proteomics across the antibody-positive, VEDOSS and established stages, showed a continuous molecular progression, with interferon and innate-immune activation already present in the antibody-positive phase. Immune dysregulation therefore begins well before classification criteria are met, defining an early window for risk stratification.
CLONALLY EXPANDED DURAL CD8+ T CELLS DRIVE LYMPHATIC REMODELLING IN NEUROPSYCHIATRIC SLE
Abstract format and assignment number: Oral presentation, OP0149
Presenting author: Y. Feng (China)
Neuropsychiatric SLE is severe and mechanistically poorly understood. In lupus-prone mice, clonally expanded dural CD8+ T cells drove meningeal lymphatic remodelling by reprogramming macrophages via GZMK to release VEGF-C; the expanded lymphatics in turn accelerated CNS antigen drainage, feeding further local clonal expansion in a selfamplifying loop. Depleting these T cells or blocking CCR5 broke the circuit, marking this T-cell–macrophage–lymphatic axis as a candidate therapeutic target in NPSLE.
GUT MICROBIOTA DYNAMICS AFTER CD19 CAR T-CELL THERAPY IN AUTOIMMUNE DISEASE
Abstract format and assignment number: Oral presentation, OP0152
Presenting author: Y. Maeda (Germany)
CD19 CAR T-cell therapy induces deep remission in autoimmune disease, but its effects beyond B cells are largely unknown. Six months after infusion the gut microbiome shifted, with loss of Bifidobacterium adolescentis and reduced faecal and anti-commensal IgA, most notably in SLE. Beyond depleting B cells, CAR T-cell therapy reshapes the gut microbiome and mucosal immunity, pointing to additional mechanisms behind its durable effect in autoimmune disease.
INTEGRATED GENOMICS AND SINGLE-CELL TRANSCRIPTOMICS DEFINE MONOCYTE-DRIVEN TISSUE INJURY IN MYOSITIS
Abstract format and assignment number: Oral presentation, OP0165
Presenting author: S. Izuka (Japan)
Myositis is classified by autoantibodies, but organ damage and treatment response often cross those lines. Integrating whole-genome and single-cell sequencing across roughly 180 patients localised genetic risk to IL1B+ classical monocytes, which were expanded in every subgroup, enriched in muscle, and linked to disease activity. This points to inflammatory monocytes as a shared driver of muscle injury beyond antibody class, and a target current classification overlooks.
Dr Hannah den Braanker, MD/PhD, Rheumatology Fellow, Post-doctoral researcher, Rotterdam
Country: Netherlands
Hannah is a rheumatology resident and clinician-scientist at Erasmus MC, Rotterdam, the Netherlands. Her research focuses on the pathogenic mechanisms behind the interplay between obesity and inflammatory arthritis, with a focus on lymphatic biology and immune cell interactions. She is a member of the Dutch Society for Rheumatology (NVR) and GRAPPA. Hannah is a member of the EMEUNET Newsletter sub-committee and Country Liaison for the Netherlands.