Analyzing Specific Pathways in Cells to Prevent Relapse in NMOSD: Shuhei Nishiyama, MD, PhD
The research fellow at the Neuroimmunology Clinic and Research Laboratory, Massachusetts General Hospital and Harvard Medical School, talked about his research of cell function in NMOSD to be presented at the upcoming AAN annual meeting. [WATCH TIME: 6 minutes]
WATCH TIME: 6 minutes
“We're going to present the data on inflammatory cytokines like IL-6 and IL-17A, which are significantly upregulated in patients with NMOSD. We can help each other to analyze more specific pathways with inflammatory causes and stop the NMOSD relapse.”
In
Results from the study supported an immunopathogenesis model in which complement pathway activation in NK and NKT cells upregulate CD16 expression that binds to antibody/antigen complexes, which may be responsible for the escalating autoimmune activity. Lead author
Prior to the meeting, Nishiyama recently sat down with NeurologyLive® in an interview to talk about his research in NMOSD. He briefly spoke about the main findings from the study and compared it with previous research results. He also shared what he is excited about regarding presenting the data at the meeting and what should be the focus for future research in the field of NMOSD.
REFERENCES
1. Nishiyama S, Wright A, Lotan I, Paul F, Levy M. Upregulated complement receptors correlate with Fc gamma receptor 3A-positive natural killer (NK) and natural killer-T (NKT) cells in neuromyelitis optica spectrum disorder. Presented at: 2023 AAN Annual Meeting; April 22-27, Boston, Massachusetts. Autoimmune Neurology: NMOSD session.
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