I am a fifth-year PhD student at the Ludwig-Maximilians-University of Munich, Germany, specializing on neuroimmunology under the mentorship of PD Dr. Simone Mader and Prof. Dr. Edgar Meinl. My research focuses on autoantibodies in inflammatory diseases of the central nervous system. The Hong Kong Laureate Forum is a global platform for scientists to share knowledge and ideas. This year, Professors Kazutoshi Mori and Peter Walter join as Laureates, honored for discovering the Unfolded Protein Response, which regulates protein production in the endoplasmic reticulum. Disruptions in this process can impair plasma cell differentiation and contribute to immune disorders. Attending this forum will provide me with a tremendous opportunity to gain insights into the UPR, and receive feedback from experts across disciplines, deepening my understanding of neuronal and immune cell biology and the pathogenesis of autoantibodies produced by plasma cells, which may inspire innovative diagnostic and therapeutic strategies. I would benefit from the valuable experience crucial for both the final stage of my PhD and my future academic career. I also highly appreciated the forum’s commitment to engaging high school students in science. With years of study abroad experience, I hope to inspire future generations to pursue their dreams in science.

Institute of Clinical Neuroimmunology, Ludwig-Maximilians University Munich

Department of Chemistry, City University of Hong Kong

Recommendation_Letter_2025_CityU_Tam.pdf

Neuromyelitis optica spectrum disorders (NMOSD) are rare inflammatory diseases of the central nervous system. Once considered a subtype of multiple sclerosis (MS), NMOSD is now recognized as a distinct condition based on clinical data and phenotypic differences. A major breakthrough was the discovery of aquaporin-4 (AQP4) immunoglobulin G (IgG) antibodies, present in approximately 80% of the patients. Additionally, antibodies against myelin oligodendrocyte glycoprotein (MOG) define a separate group known as MOG-antibody associated disease (MOGAD).
Towards recognizing new autoantigens, we identified a novel autoantigen in a subset of patients by proteomic array who were tested negative for antibodies to AQP4 and MOG. Those novel antibodies in patient samples were further verified with cell-based assay, western blot and immunohistochemistry. Four patients were identified with the novel antibody who presented similar but atypical MS and NMOSD clinical phenotypes. By using self-generated monoclonal antibody, we showed pathogenicity in an in vivo rodent model. Our findings may serve as an important biomarker, provide greater insight into the disease pathogenesis of the CNS demyelinating diseases, while also improving the likelihood of facilitating early and effective therapeutic interventions for patients.