Ahmet Gül

Professor Ahmet Gül graduated from the Istanbul Faculty of Medicine at Istanbul University, where he also completed his training in internal medicine and rheumatology. He has been serving on the faculty of the same institution since 1997. His research focuses on the immunopathogenesis and genetics of inflammatory rheumatic disorders, particularly Behçet’s disease, familial Mediterranean fever (FMF), and other monogenic autoinflammatory conditions, as well as on drug development in these areas. He has conducted research at the Karolinska Institute (Stockholm, Sweden) and the ARC Epidemiology Research Unit (Manchester, UK), and he currently collaborates with the National Institutes of Health (USA) on the genetics of Behçet’s disease. Professor Gül is an active member of several professional societies, including the Turkish Society for Rheumatology, the Turkish Society of Immunology, the Behçet’s Disease Society of Turkey (currently serving as President), the International Society for Behçet’s Disease (currently President-Elect), and the International Society of Systemic Auto-Inflammatory Diseases. He has authored over 200 scientific papers in peer-reviewed journals, with more than 14,000 citations and an h-index of 61 (WoS AAT-7787-2020) and 65 (Scopus). He also serves on the editorial boards of prestigious rheumatology journals, including Annals of the Rheumatic Diseases and special issues of Clinical and Experimental Rheumatology focused on Behçet’s disease and other autoinflammatory conditions. Professor Gül’s current research interests include: • The immunogenetic basis of Behçet’s disease, particularly pathogenic mechanisms linked to HLA Class I and ERAP1 interactions, as well as non-HLA genetic variations • Pyrin-mediated inflammatory mechanisms in FMF • Mechanisms of action of colchicine in FMF and other inflammasomopathies • Inflammatory dynamics in autoinflammatory disorders • Development of biomarkers for refractory disease in IL-1–driven disorders • Pathogenic mechanisms underlying AA amyloidosis • COVID-19 and inflammasome-associated hyperinflammatory responses