Ahmet Gül, M.D.

Professor of Medicine

Istanbul University, Istanbul Faculty of Medicine

Department of Internal Medicine, Division of Rheumatology

Professor Ahmet Gül graduated from Istanbul Faculty of Medicine of Istanbul University. He completed his training in internal medicine and rheumatology at the same institution; and he has been serving on its faculty since 1997.

His research has been focused on the immunopathogenesis and genetics of inflammatory rheumatic disorders, especially Behçet’s disease, familial Mediterranean fever (FMF), and other monogenic autoinflammatory disorders as well as drug development. He carried out research at Karolinska Institute (Stockholm, Sweden) and ARC Epidemiology Research Unit (Manchester, UK), he has currently been collaborating with the National Institutes of Health (USA) on the genetics of Behçet’s disease.

He is a member of several professional societies including Turkish Society for Rheumatology, Turkish Society of Immunology, Behçet’s Disease Society of Turkey (currently President), International Society for Behçet’s Disease (currently Vice President), and International Society of Systemic Auto-Inflammatory Diseases.

He has over 200 scientific papers in peer-reviewed journals and more than 14,000 citations with an h index of 59 (Publons ID AAT-7787-2020), and he has been serving on the Editorial Board of prestigious rheumatology journals including the Annals of the Rheumatic Diseases and “Behçet’s disease and other autoinflammatory conditions”issues of Clinical and Experimental Rheumatology. 

Professor Gül’s active immunological research is focused on:

Immunogenetic basis of Behçet disease, especially pathogenic mechanisms associated with HLA Class I and ERAP1 interactions as well as with non-HLA genetic variations

- Pyrin mediated inflammatory mechanisms in FMF

- Mechanism of action of colchicine in FMF and other inflammasomopathies

- Inflammatory dynamics of autoinflammatory disorders

- Development of biomarkers to define refractory disease in IL-1-driven disorders

- Pathogenic mechanisms associated with AA amyloidosis

- COVID-19 and inflammasome-associated hyperinflammatory response