Claudia Iannone
Claudia is a Rheumatology resident at Milan University, carrying out her research at Gaetano-Pini Hospital in Milan, Italy. Her research interests are focused systemic sclerosis, Interstital lung disease in rheumatic diseases and vasculitis. She is a member of EULAR lung study group and of EUSTAR YIG. Claudia is part of the social media subcommittee
| Poster 0019 | Sunday, 26.10.2025 10:30 -12:30 Abstract Session: Genetics, Genomics & Proteomics Presenting author: A Gómez Gómez (Spain) Title: Single cell characterization of the circulating immune system in Sjögren’s Syndrome  This study assessed circulating immune cells in 32 Sjögren’s syndrome patients versus 10 controls using single-cell transcriptomics of 198,078 cells. SS showed increased CD4+ TH2, CD8+ TEM, and proliferative T cells, but decreased naive T cells, MAIT, pDC, DC3, and memory B cells. A novel CD8+ T cell subpopulation enriched for SS-risk genes was identified. Strong interferon-response signatures and cell-specific aberrant regulatory changes were observed across multiple cell types. Providing the largest single-cell atlas of circulating immunity in SS to date, this work reveals novel disease-associated cell populations with potential diagnostic value. |
| Oral Presentation 2584 | Tuesday, 28.10.2025 14:15 Abstract Session: Innate Immunity Presenting author: L Dionet (France) Title: Spatially Resolved Transcriptomics Reveal Macrophage Heterogeneity in Giant Cell Arteritis This study assessed macrophage heterogeneity in Giant Cell Arteritis using spatial transcriptomics. TREM-1 signalling emerged as a top upregulated pathway in media-infiltrating macrophages, with inflammatory SPP1+ TREM1+ macrophages in the media and TREM2+ macrophages near myofibroblasts. Serum sTREM-1 levels correlated with CRP and IL-6. TREM-1 inhibitor nangibotide reduced monocyte migration and NFkB activation, positioning TREM-1 as a promising therapeutic target in GCA. The spatial resolution approach uniquely identifies distinct macrophage subsets with different therapeutic potential, particularly highlighting TREM-1 as a novel druggable target in GCA. |
| Poster 0942 | Monday, 27.10.2025 10:30 -12:30 Abstract Session: Systemic Lupus Erythematosus – Animal Models Presenting author: J Nicholson (USA) Title: Sodium-Glucose Co-Transporter 2 Inhibitors Modulate Renal Injury and Autoreactive Plasma Cells in Lupus This study assessed SGLT2 inhibitor effects in lupus-prone MRL/lpr and NZB/NZW mice. Dapagliflozin reduced autoreactive plasma cells in spleen, bone marrow, and kidneys, inhibited germinal centers and plasmablast generation, and increased regulatory T cells systemically. Periarterial inflammation and interstitial fibrosis were significantly ameliorated. The glucose metabolism shift induced by SGLT2i may drive decreased autoimmunity, positioning these drugs as novel lupus therapeutics. Revealing unexpected immunomodulatory effects beyond their renal protective mechanisms, SGLT2 inhibitors may offer a repurposing opportunity for lupus treatment. |
| Oral Presentation 2584 | Tuesday, 28.10.2025 14:15 Abstract Session: Innate Immunity Poster 0914 | Monday, 27.10.2025 10:30 -12:30 Abstract Session: B Cell Biology & Targets in Autoimmune Disease Presenting author: X Wu (USA) Title: Preclinical Expansion of Autoreactive Naive B cells Drives RA onset in ACPA+ individuals This interesting study assessed preclinical immunologic events in ACPA+ individuals who progressed to RA. Single-cell profiling revealed marked expansion of IGHM+ IGHD+ CXCR5+ CD69+ activated naive B cells in converters, exhibiting pro-inflammatory transcriptional profiles and elevated clonal diversity. Recombinant antibodies from these cells demonstrated broad autoreactivity to RA-associated autoantigens. This autoreactive IgM pool may drive early immunologic activation and eventual RA onset, offering predictive biomarkers. This study is interesting because it identifies a specific pre-clinical B cell signature that predicts RA development in at-risk individuals. The identification of a specific pre-clinical B cell signature predicting RA development in at-risk individuals opens new avenues for preventive interventions. |
| Poster 0953 | Monday, 27.10.2025 10:30 -12:30 Abstract Session: Systemic Lupus Erythematosus – Animal Models Presenting author: R Weissman-Tsukamoto (USA) Title: NMDAR Autoantibody-Induced Neuronal Damage in the Amygdala Mediates Mood and Anxiety Disorders in a Model of Neuropsychiatric Lupus This study assessed chronic effects of anti-NMDAR antibodies in neuropsychiatric lupus. Epinephrine caused selective blood-brain barrier breach in the amygdala, enabling antibody penetration. Significant neuronal loss occurred in basolateral and lateral amygdala nuclei, correlating with anxiety behaviors. Surviving neurons showed abnormal morphology and lipid oxidation suggesting ferroptosis, differing from hippocampal pathology. This reveals distinct neuropathological mechanisms underlying psychiatric symptoms in NPSLE. This study is interesting because it demonstrates region-specific neuronal damage mechanisms that could explain the varied psychiatric manifestations in lupus patients, which are the most difficult to address and treat at the moment. |
| Oral Presentation 1757 | Tuesday, 28.10.2025 11:15 Abstract Session: Spondyloarthritis – Basic Science Presenting author: M Raimondo (Germany) Title: Skin-to-Joint Immune Cell Migration and Synovial Reprogramming in Psoriatic Arthritis Onset This interesting study assessed skin-joint axis mechanisms in PsA using IL-23 overexpression KAEDE mice with photo-conversion tracking. Skin-derived CD2+MHCII+ myeloid progenitors migrated to synovium, differentiating into pro-inflammatory macrophages in susceptible mice but M2-like cells in resistant mice. CD200+ synovial fibroblasts emerged as key modulators promoting protective responses. Mitochondrial DNA sequencing validated skin origin of synovial myeloid cells in human early PsA patients. Providing first direct evidence of functional skin-to-joint immune cell migration in humans through innovative tracking methods, this work reveals fibroblast-mediated control mechanisms that determine arthritis susceptibility in psoriasis patients. |
| Poster 0956 | Monday, 27.10.2025 10:30 -12:30 Abstract Session: Systemic Sclerosis – Basic Science Presenting author: A Matei (Germany) Title: Mapping Metabolic Changes in Skin Fibrosis in Systemic Sclerosis by Spatial Proteomics This interesting study assessed metabolic profiles in SSc skin using imaging mass cytometry with 38 metal-labeled antibodies targeting metabolic enzymes. Progressive SSc patients showed distinct metabolic regulomes with upregulated glycolysis and TCA/OXPHOS scores. A metabolically active fibroblast subset expressing high αSMA and FAP was enriched in progressive disease, forming niches with similarly metabolic endothelial cells and macrophages. Metabolic phenotyping may identify patients at progression risk. The discovery of metabolically-defined fibroblast niches through spatial proteomics offers a novel biomarker approach for identifying patients at risk for progressive skin fibrosis. |
| Poster 0114 | Sunday, 26.10.2025 10:30 – 12:30 Abstract Session: Spondyloarthritis – Basic Science Presenting author: S Hilliquin (France) Title: A Rare Variant in the extl3 Gene Is Associated with Altered Wnt Signaling Pathway in a Novel Mouse Model of Axial Spondyloarthritis This interesting study assessed Wnt signaling in Extl3mut/+ mice developing sacroiliac joint lesions resembling axSpA. Tcf1 immunostaining increased markedly in chondrocyte columns and subchondral bone. RNA-seq revealed downregulation of Wnt inhibitors Dkk-1 and Sclerostin, with overexpression of β-catenin and Tcf7. Notably, Wnt pathway inhibition with Dkk-1 reversed the phenotypes, including delayed osteoblast and accelerated chondrocyte differentiation, highlighting potential therapeutic targets for AS ossification. Linking a rare EXTL3 variant to disrupted Wnt signaling in a novel mouse model reinforces the pathway’s critical role in AS pathological ossification and validates Wnt modulation as a therapeutic strategy. |