Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, United States; The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, United States; Department of Neurology, The Ohio State University College of Medicine, Columbus, United States
Riley B Catenacci
Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, United States; The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, United States
Matthew D Smith
Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, United States
Dongeun Heo
The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, United States
The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, United States; The Kavli Neuroscience Discovery Institute, Johns Hopkins University, Baltimore, United States
Peter A Calabresi
Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, United States; The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, United States
Oligodendrocytes and their progenitors upregulate MHC pathways in response to inflammation, but the frequency of this phenotypic change is unknown and the features of these immune oligodendroglia are poorly defined. We generated MHC class I and II transgenic reporter mice to define their dynamics in response to inflammatory demyelination, providing a means to monitor MHC activation in diverse cell types in living mice and define their roles in aging, injury, and disease.
