JOURNAL OF IIMER May 2026 The session is moderated by Associate Professor Eva Untersmayr-Elsenhuber, a specialist in immunology and head of the Gastrointestinal Immunology research group at the Medical University of Vienna. A member of EMERG, her extensive research background in food allergy, gastrointestinal immunology and pathophysiology brings a broad immunological perspective to the session. Professor Leo Joosten of Radboud University Medical Centre in Nijmegen focuses on host defence mechanisms and the chronic inflammation that can follow pathogen exposure. His work on innate immune receptors, the inflammasome and Lyme disease pathogenesis is directly relevant to the question of how an initial infection can set in motion a sustained immune response. At BRMEC15 he will present on innate immunity and post-infectious immune dysregulation, and the insights this offers for ME research. Professor Sonya Marshall-Gradisnik, Director of the National Centre for Neuroimmunology and Emerging Diseases (NCNED) at Griffith University, Australia, is one of the world's leading ME researchers. Her laboratory has pioneered work on natural killer cell dysfunction and calcium ion channel dysregulation in ME, and has demonstrated significant overlaps between ME and long COVID in immune cell dysfunction and symptom presentation. At BRMEC15 she will present on ion channels, calcium signalling and inner cell function - work that sits at the intersection of immunology and cell biology. Marcus Buggert, Associate Professor Marcus Buggert, Center for Infectious Medicine, Karolinska Institutet studies human adaptive immunity to viral infections across blood and tissue compartments. His research on antigen-specific T cells and tissue-based immunology has informed understanding of how immune responses persist and become dysfunctional following infection. At BRMEC15 he will present on tissue-specific immune dysregulation in long COVID - findings with clear implications for ME. Session 6: Metabolism Metabolic dysfunction is increasingly recognised as a central feature of ME. Studies have identified abnormalities in energy metabolism, mitochondrial function, fatty acid oxidation and cellular oxygen utilisation in ME patients. These findings point towards a disease in which the body's ability to generate and use energy at the cellular level is fundamentally compromised - a hypothesis that may explain the post-exertional malaise that is the hallmark symptom of ME, and which distinguishes it from other conditions characterised by fatigue. Moderated by Associate Professor Rikke Katrine Jentoft Olsen, Aarhus University, Denmark / EMERG Invest in ME Research Page 27 of 35
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