Dr Fatma Gül Demirkan
Country: Türkiye
Dr. Demirkan is an Associate Professor and pediatric rheumatologist at Kanuni Sultan Süleyman Training and Research Hospital in Istanbul, Türkiye. She is currently pursuing her MSc in Autoinflammatory Diseases in Children (thesis program) at İstanbul University, İstanbul Faculty of Medicine.
Her clinical and research interests focus on autoinflammatory and autoimmune diseases in children, including familial Mediterranean fever, juvenile idiopathic arthritis, and systemic lupus erythematosus. She serves as the Clinical Lead of the PReS EMERGE Research Subcommittee and participates in several international multicenter collaborations. Dr. Demirkan is a member of the Pediatric Rheumatology European Society (PReS), EMEUNET (social media subcommittee) and PRINTO networks.
| Poster 0076| Sunday, 08.11.2026 10:30–12:30 Session: Spondyloarthritis Including Psoriatic Arthritis – Basic and Translational Science Poster A (0069-0077) Presenting author: Semini Beragama Jathunga (Canada) Title: Sex-Specific Biomarkers in the Transition to PsA: Longitudinal Metabolomic Analyses  This longitudinal study identified sex-specific metabolic changes accompanying the transition from psoriasis to psoriatic arthritis. Alterations involved inflammatory lipid signalling and mitochondrial function, with greater amino acid disturbances in males and lipid changes in females. These findings highlight potential biomarkers for earlier detection and sex-informed risk assessment, pending validation. |
| Poster 0026| Sunday, 08.11.2026 10:30–12:30 Session: Systemic Sclerosis & Related Disorders – Basic and Translational Science Poster A (0022-0038) Presenting author: Neha Khanna (USA) Title: Defining the role of TEADs and VGLL3 in scleroderma endothelial cells This experimental study identified TEAD3 and VGLL3 as key regulators of endothelial-to-mesenchymal transition in systemic sclerosis. Silencing either factor reduced profibrotic markers and improved angiogenic capacity, highlighting potential therapeutic targets to preserve endothelial function and limit fibrosis-associated vascular injury. |
| Poster 0008| Sunday, 08.11.2026 10:30–12:30 Session: Vasculitis – Basic and Translational Science Poster A (0001-0008) Presenting author: Ingrid Lindquist (USA) Title: Transcriptome analysis of temporal artery and aortic lesions highlights vessel-specific chemotaxis and cell adhesion in GCA This transcriptomic study revealed vessel-specific chemotaxis and cell adhesion signatures in giant cell arteritis, highlighting CCL22 in temporal arteries and CXCL13 in aortic lesions. These findings may help explain distinct patterns of vascular involvement and guide the development of biomarkers and targeted therapies. |
| Poster 0070| Sunday, 08.11.2026 10:30–12:30 Session: Spondyloarthritis Including Psoriatic Arthritis – Basic and Translational Science Poster A (0069-0077) Presenting author: Thomas Macleod (United Kingdom) Title: Dual IL-17A/IL-17F Inhibition Modulates Entheseal Stromal Inflammatory Networks and Reveals a Role for IL-17F in Neutrophil Recruitment in Human Entheseal Inflammation. This experimental study showed that dual IL-17A/IL-17F blockade with sonelokimab more broadly suppressed entheseal stromal inflammatory pathways than IL-17A inhibition alone, reducing neutrophil recruitment and degranulation. These findings highlight IL-17F as a contributor to persistent entheseal inflammation and provide a mechanistic rationale for dual inhibition. |
| Poster 0117| Sunday, 08.11.2026 10:30–12:30 Session: Muscle Biology, Myositis, & Myopathies – Basic and Translational Science Poster A (0117-0120) Presenting author: Karen Gambina (USA) Title: A Population of CD57⁺ CD8⁺ T Cells With Cytotoxic Potential Are Expanded in Immune-Mediated Necrotizing Myopathy and Dermatomyositis This exploratory study identified expanded CD57⁺ CD8⁺ T-cell populations with cytotoxic potential in immune-mediated necrotizing myopathy and dermatomyositis, including during clinical remission. These findings suggest persistent immune abnormalities despite apparent disease inactivity and highlight the need to investigate their role in muscle injury and future flares. |