Poster abstracts
Poster number 75 submitted by Jack Bozik
Oligodendrocyte derived serine protease inhibitor Serpina3n modulates neuroinflammation during EAE
Jack B. Bozik MS (Department of Neurology, College of Medicine, The Ohio State University), Michelle Wedemeyer MD, PhD (Department of Neurosurgery, Nationwide Childrens Hospital), Amy Webb Hite PhD (Department of Biomedical Informatics, The Ohio State University), Cole A. Harrington MD, PhD
Abstract:
Multiple sclerosis (MS) is an autoimmune demyelinating disease that damages glial cells throughout the CNS. Oligodendroglia, cells responsible for producing myelin sheaths that wrap around neuronal axons are damaged by the infiltrating T cells. However, subsets of oligodendroglia have been characterized to express immunoregulatory molecules. One of the transcripts these immune oligodendroglia (iOPC/iOL) upregulate is serine protease inhibitor Serpina3n. Typically released into the bloodstream in response to general inflammation, the role of Serpina3n in the CNS is not well understood and its release by oligodendroglia during neuroinflammation is a novel subject, which we aim to better understand using a conditional knockout (cKO) murine line as well as Th17 adoptive transfer to model MS.
Naive CNS tissue sees limited Serpina3n expression due to the lack of activate immune cells for Serpina3n to respond against. However, during Th17 adoptive transfer Serpina3n+ cells were highly elevated in the brain and spinal cord. In oligodendrocyte specific Serpina3n cKO mice which experienced Th17 adoptive transfer, disease onset developed sooner and peak severity of disease phenotypes was significantly higher compared to wild type mice which experienced adoptive transfer. The spinal cord of Serpina3n cKO mice also saw an increased loss of Sox10+ cells compared to the wild type adoptive transfer mice. Upregulation of neuroprotective molecules like Serpina3n seems to contribute to mouse survival, lesion size, and OPC persistence within the inflammatory lesion environment both in young and aged animals.
References:
None
Keywords: Neuroscience, Immunology, Cell Biology