Influx of T cells into corpus callosum increases axonal injury, but does not change the course of remyelination in toxic demyelination

Multiple sclerosis (MS) is a focal inflammatory and demyelinating disease. The inflammatory infiltrates consist of macrophages/microglia, T and B cells. Remyelination (RM) is an endogenous repair process which frequently fails in MS patients. In earlier studies, T cells either promoted or impaired RM. Here, we used the combined cuprizone/MOG-EAE model to further dissect the functional role of T cells for RM. The combination of MOG immunization with cuprizone feeding targeted T cells to the corpus callosum and increased the extent of axonal injury. Global gene expression analyses demonstrated significant changes in the inflammatory environment; however, additional MOG immunization did not alter the course of RM. Our results suggest that the inflammatory environment in the combined model affects axons and oligodendrocytes differently and that oligodendroglial lineage cells might be less susceptible to T cell mediated injury.

Automated summary

Multiple sclerosis (MS) is a focal inflammatory and demyelinating disease characterized by the infiltration of macrophages/microglia, T and B cells. Remyelination (RM) is an endogenous repair process that often fails in MS patients. In this study, the combination of cuprizone feeding and MOG immunization targeted T cells to the corpus callosum and increased axonal injury, but did not alter the course of RM. Our results suggest that the inflammatory environment affects axons and oligodendrocytes differently, and oligodendroglial lineage cells may be less susceptible to T cell mediated injury.