MHC class I and MHC class II reporter mice enable analysis of immune oligodendroglia in mouse models of multiple sclerosis
Abstract
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.
Data availability
Sequencing data has been deposited in GEO under the accession code GSE213739Code used to analyze sequencing data was uploaded at Source Code File 1All data generated or analyzed during this study are included in manuscript source data files
Article and author information
Author details
Funding
National Institutes of Health (NIA AG072305)
- Dwight E Bergles
National Multiple Sclerosis Society (FAN-1707-28857)
- Em P Harrington
Dr. Miriam and Sheldon G Adelson Medical Research Foundation
- Dwight E Bergles
National Science Foundation
- Riley B Catenacci
National Institutes of Health (R01 NS041435)
- Peter A Calabresi
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Reviewing Editor
- Tatyana Chtanova, Garvan Institute of Medical Research, Australia
Ethics
Animal experimentation: All animal procedures were performed according to protocols approved by the Johns Hopkins Animal Care and Use Committee protocol #MO22M158.
Version history
- Received: August 24, 2022
- Preprint posted: September 28, 2022 (view preprint)
- Accepted: April 13, 2023
- Accepted Manuscript published: April 14, 2023 (version 1)
- Version of Record published: May 12, 2023 (version 2)
Copyright
© 2023, Harrington et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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