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SUMMARY:[The Svedberg seminar] - Human beta cell protection by Nature
DESCRIPTION:Bart RoepProfessorLeiden University Medical Center\, Netherlands \n\n\n\n \n\n\n\n \n\n\n\nBio\n\n\n\nBart Roep is Professor of Medicine & Professor of Diabetology\, Immunopathology and Intervention at the Department of Internal Medicine\, Leiden University Medical Center\, Leiden\, Netherlands\, where he heads the Section Immuno-modulation & Regenerative Medicine. He studied Medicine and Life Sciences at the University of Amsterdam and obtained his PhD in Medicine at Leiden University. He pioneered studies on the role of T-cells in the pathogenesis of T1D and discovered some of their targets in β-cells\, provided seminal proof of their role in human β-cell destruction and defined immune correlates of disease progression and therapeutic intervention. He contributed to a suite of clinical intervention trials in T1D\, including pioneering strategies on tissue-specific tolerance induction\, regenerative medicine\, gene and stem cell therapy\, faecal microbiome transplantation and β-cell replacement therapies (pancreatic donor islets and embryonic stem cell derived β-cell progenitors). A profound twist in prevalent belief of the immunopathogenesis involved his discovery of the role of β-cells in their own demise. His current focus is on regenerative medicine in T1D from an immunological perspective. \n\n\n\nHuman beta cell protection by Nature\n\n\n\nType 1 diabetes results from an autoimmune mediated destruction of the insulin-producing β-cells in the pancreatic islets of Langerhans in people with genetic predisposition to develop this disease. Insulin gene (INS) variation and beta-cell stress associate with risk for development of type 1 diabetes  (T1D) and autoimmunity against insulin. We discovered the relationship between ER stress and insulin mRNA from INS risk variants in human β-cells\, and how this variation relates to β-cells function\, stress and immunogenicity. This novel explanation for genetic protection from T1D inferred by INS polymorphism\, puts β-cells in the center of T1D pathogenesis. Beta cells carrying this particular protective INSP variant can alleviate ER stress by insulin mRNA decay\, resulting in reduced immunogenicity and improved islet function. We propose that INSP is a causal variant contributing to genetic protection from T1D. The clinical and therapeutic implications of this discovery will be discussed. \n\n\n\n \n\n\n\n \n\n\n\n \n\n\n\n\n\n\n\nHost: Olov Andersson olov.andersson@mcb.uu.se\, UU
URL:https://www.scilifelab.se/event/the-svedberg-seminar-bart-roep/
LOCATION:BMC Room C8:301\, Husargatan 3\, Uppsala\, Sweden
CATEGORIES:Event
ATTACH;FMTTYPE=image/png:https://www.scilifelab.se/wp-content/uploads/2022/02/Picture1-The-Svedberg.png
ORGANIZER;CN="The Svedberg Seminar Series":MAILTO:thesvedberg@scilifelab.uu.se
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